Scottish Doctor, author, speaker, sceptic

Very high LDL and no cardiovascular disease – at all!

If your hypothesis is that all swans are white, the discovery of one black swan refutes your hypothesis. That is how science works. Or at least that is how science should work. In the real world, scientists are highly adept at explaining away contradictions to their favoured hypotheses. They will use phrases such as, it’s a paradox. Or, inform you that you didn’t measure the correct things, or there are many other confounding factors – and suchlike.

Anyway, accepting that the finding of someone with a very high LDL level, and no detectable atherosclerosis, will always be dismissed – in one way or another – I am still going to introduce you to a ‘case history’ of a seventy-two-year-old man with familial hypercholesterolaemia, who has been studied for many, many, years. Try as they might, the researchers have been unable to discover any evidence for cardiovascular disease (CVD) – of any sort.

In the past, I have spoken to many people with very high LDL and/or total cholesterol levels who are CVD free, even in very old age. The mother of a friend of mine has a total cholesterol of level of 12.5mmol/l (483mg/dl). She is eighty-five, continues to play golf and has not suffered from any cardiovascular problems.

However, none of these people had been studied in any detail. Which means that they can, and are, dismissed as irrelevant ‘anecdotes’. Yes, the widely used and highly exasperating phrase that I often encounter is that ‘the plural of anecdote is not data’. This, of course, is completely untrue, or at least it is untrue if you start dismissing detailed individual cases as anecdote.

Whilst an anecdote may simply be a story, often second hand, a case history represents a painstaking medical history, including biochemical and physiological data. In reality, the plural of case histories is data. That is how medicine began, and how most medical breakthroughs have been made. We look at what happens to real people, over time, we study them, and from this we can create our hypotheses as to how diseases may be caused and may then be cured.

So, a single case is NOT an anecdote, and cannot be lightly dismissed with a wave of the hand and a supercilious smirk.

In fact, the man who is the subject of this case history has written to me on a few occasions, to tell me his story. I have not written anything about him before, as I knew his case was going to be published, and I did not want to stand on anyone’s toes. With that in mind, here we go.

The paper was called ‘A 72-Year-Old Patient with Longstanding, Untreated Familial Hypercholesterolemia but no Coronary Artery Calcification: A Case Report.’ 1

The subject has a longstanding history of hypercholesterolemia. He was initially diagnosed while in his first or second year as a college student after presenting with corneal arcus and LDL-C levels above 300 mg/dL [7.7mmol/l]

He reports that pharmacologic therapy with statins was largely ineffective at reducing his LDL-C levels, with the majority of lab results reporting results above 300 mg/dL and a single lowest value of 260 mg/dL while on combination atorvastatin and niacin. In addition to FH-directed therapy, our subject reports occasionally using baby aspirin (81 mg) and over-the-counter Vitamin D supplements and multivitamins.

In the early 1990s, our patient underwent electron beam computed tomography (EBCT) imaging for CAC following a series of elevated lipid panels. Presence of CAC (coronary artery calcification) was assessed in the left main, left anterior descending, left circumflex, and right coronary arteries and scored using the Agatston score.

His initial score was 0.0, implying a greater than 95% chance of absence of coronary artery disease. Because of this surprising finding, he subsequently undertook four additional EBCT tests from 2006 to 2014 resulting in Agatston scores of 1.6, 2.1, 0.0, and 0.0, suggesting a nearly complete absence of any coronary artery calcification. In February of 2018, he underwent multi-slice CT which revealed a complete absence of coronary artery calcification.

So, here we have a man who has an LDL consistently three to four times above ‘average’. He had tried various LDL lowering agents over the years. None of which had done anything much to lower LDL. Therefore, his average LDL level over a twenty-year period has been 486mg/dl (12.6mmol/l.

Despite this he has absolutely no signs of atherosclerotic plaque, in any artery, no symptoms of CVD and is – to all intents and purposes – CVD free. What of his relatives? If he has FH, so will many others in his family.

‘He has one sister three years his senior who also has FH and a history of high lipid levels. She also has no history of myocardial infarction, angina, or other symptoms of coronary artery disease. His mother had FH, although she died of pancreatic cancer at age 77. She and her three siblings were never treated for, and had no history of, cardiovascular disease. The patient reports that his father had one high cholesterol score (290s), but was never diagnosed with FH, had no history of cardiovascular disease and died in his 80s during surgery for hernia repair.’

What to make of this? Well, I know that the ‘experts’ in cardiology will simply ignore this finding. They prefer to use the ‘one swallow does not a summer make’ approach to cases like this. For myself I prefer the black swan approach to science. If your hypothesis is that a raised LDL causes CVD, then finding someone with extremely high LDL, and no CVD, refutes your hypothesis.

Unfortunately, but predictably, the authors of the paper have not questioned the LDL approach. Instead, they fully accept that LDL does cause CVD. So, this this man must represent ‘a paradox’. They have phrased it thus:

‘Further efforts are underway to interrogate why our patient has escaped the damaging consequences of familial hypercholesterolemia and could inform future efforts in drug discovery and therapy development.’

To rephrase their statement. We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him. I have an alternative, and much simpler explanation: LDL does not cause CVD. My explanation has the advantage that it fits the facts of this case perfectly, with no need to start looking for any alternative explanation.

And just in case you believe this is a single outlier, something never seen before or since. Let me introduce you to the Simon Broome registry, set up in the UK many years ago to study what happens to individuals diagnosed with familial hypercholesterolaemia (FH). It is the longest, if not the largest, study on FH in the world.

It has mainly been used as one of the pillars in support of the cholesterol hypothesis. However, when you start to look closely at it – fascinating things emerge. One of the most interesting is that people with FH have a lower than expected overall mortality rate – in comparison to the ‘normal’ population. Or, to put this another way. If you have FH, you live longer than the average person.

Even if we look at death from heart disease (those with FH have never been found to have an increased rate of stroke) we find that in the older population, the rate of death from Coronary Heart Disease (CHD) was actually lower than the surrounding population in some age groups.

For instance, in the male population aged 60 – 79 (who were CHD free on entry to the study) the rate of death from heart attacks was lower than the surrounding population. Not significantly, but it certainly was not higher.

In fact, in the total male population aged 20 – 79 with FH, the rate of death from CHD was virtually identical to the surrounding population. Over a period of 13,717 years of observation, the expected number of fatal heart attacks was calculated to be 46. The actual observed number was 50.

In women, the expected number of heart attacks in the population aged 20 – 79 was 40, the actual number of observed fatal heart attacks was 40. Which means that FH was not found to be a risk factor for CHD in those enrolled in the study – who had no diagnosed heart disease prior to enrolment2.

Which represents, I suggest, another fully grown black swan. There you go. Two in one day.

407 thoughts on “Very high LDL and no cardiovascular disease – at all!”

Once again, thank you Dr. K. for throwing light on the mystical world of medical research and stats. I still find it amazing that the ‘high priests’ of science still act like blinkered religious zealots. One day….

“To rephrase their statement. We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him. I have an alternative, and much simpler explanation: LDL does not cause CVD. My explanation has the advantage that it fits the facts of this case perfectly, with no need to start looking for any alternative explanation”.

That convinces me.

On the other hand, as Upton Sinclair remarked about a century ago, “It is difficult to get a man to understand something when his salary depends upon his not understanding it”.

The bulk of doctors never read a paper- let alone critique it. Therefore they do not have the tools do do so. It’s a shame, some are so full of holes, or based on such a limited understanding of the potential that reading them is amusing. Then there are the studies done on only desk bound middle aged men that are supposedly representative of all of humanity that they should be considered authoritative.
Psychology studies – mostly done on young US college students keen enough for cash to take part. That group has been called “WEIRD” (Westernised, Educated, Industrialised, Rich, Democratic). Apparently they are a representative sample of the human mind though.

I’m starting to think that there should be continuing medical education in reading science papers- with the highest marks awarded for the greatest number of hits made on 100 papers. If you don’t have that kind of scoring it will be turned into a module developed by the professional colleges, funded by pharma, and neutered.

It might also be germane for Dr Kendrick to send this article to The Times:

“Tens of thousands of women with an inherited heart condition face an increased risk of dying prematurely because doctors are not giving them the best treatment, experts have warned.

In men with the condition, familial hypercholesterolaemia (FH), the risk is falling. A man with FH is 2.5 times as likely as the general population to die from heart disease, down from 4.5 times a decade ago. For women the risk has risen over the past ten years and is now six times as high as that of the general population.

Researchers from University College London said it was a “clear sign” that women with the condition were not being given the best available treatment, despite being at serious risk of a heart attack, stroke and heart disease-related death.

Experts said that there was a tendency to treat FH less aggressively in women because of an inaccurate misconception that they were at lower risk. Sufferers have high cholesterol from birth, which builds up in their arteries and they often suffer a heart attack in their 40s or 50s. Before statins were available, men with the condition were five times as likely to die from heart disease as the general population, and women seven times.

When early statins came in, between 1992 and 2008, the rates dropped for both sexes to about 4.5 times as likely. The study suggests that high-potency statins introduced between 2008 and 2015 have helped men and not women.

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Steve Humphries, the lead researcher, said: “Women with FH are often identified later in life than men, and will also have to stop taking a statin when they are trying to conceive, during pregnancy and breastfeeding.

“This means that they should be offered high-intensity statin therapy as soon as they are identified, and this seems not to be happening at the moment.” Cholesterol levels naturally rise during pregnancy, which can exacerbate the problem. Professor Humphries said that angina pains, which might indicate someone was developing heart disease, might not present as a typical pattern in women “and be missed by them or the doctor”. He added: “Another problem may be that more women are smoking than used to be the case and smoking really increases risk.”

Dr Devaki Nair, of the Royal Free hospital in London, said that the results could also suggest an “unknown interaction” between gender and the condition.

The study involved data on nearly 2,000 patients with a diagnosis of FH. There are an estimated 260,000 people in the UK with FH, the majority of whom are undiagnosed.

Sir Nilesh Samani, a professor and medical director at the British Heart Foundation (BHF), which part-funded the study, said: “This study shows the remarkable benefits that statins have had in reducing the risk from FH but also highlights that more needs to be done. In particular, the reduction in mortality in women with FH seems to be less than with men. There may be several reasons including a late diagnosis of FH in women or a tendency to treat less aggressively as women may perceived to be at lower risk.

“This study highlights that heart disease does not discriminate. The Nice guidance recommends that both men and women with FH should be treated with a high-intensity statin therapy. We need to do more to ensure the guidelines are followed, so women with FH aren’t put at unnecessary risk.”

Many people never develop signs to indicate they have FH, but classic signs include lumps and bumps around the knuckles or Achilles tendon caused by cholesterol deposits, or yellow cholesterol build-up around the eyes. The BHF recommends people ask their GP for testing if a close relative has had a heart attack at a young age — before 55 in a man and before 65 in a woman.”

It is an uphill struggle arguing against the cholesterol chd hypothesis but I keep going. We are not just disagreeing with authority – if a professor of cardiology says so it MUST be true – but we now are fighting against decades of cultural change and an almost unwillingness to think for yourself. I can spend valuable consultation minutes pointing out the weakness of the whole argument to a patient, I seem to get through, and then am asked what is her colesterol level , and is that ‘good’ or ‘bad’?

Well, whilst I was having a post NSTEMI angiogram, I was questioned why I had refused statins. I clearly made my case, which went down like a lead balloon. It was only later, when I looked up the cardiologist in question that I realised that I had been arguing with a cardiac pharmacologist. Oops

Dr Kendrick
Fascinating. I have family members with high cholesterol and assumed FH. Assumed because they have not been genetically tested for FH. They take statins and assume that all is now good. However, carbs and beer are the mainstay of their diet – and it is visible. So they may die of CVD CAD etc. and FH will be blamed.
Are your references above to genetically tested FH or assumed FH as cholesterol is high?
Thanks and appreciations as always

The diagnoses of FH is still (as far as I am aware) made on LDL level. In the Simon Broome registry many are genetically tested (?all of them), mainly to trace relatives. The individual case has been tested in every way.

I am a 33 year old woman who was diagnosed with FH by my cardiologist when I was 23 years old. He based this diagnosis on my LDL levels (as well as lipoprotein a and ApoB) and my family history (father died of heart attack at 56). He also diagnosed my sister using the same criteria but never tested us for the gene mutation. We were both prescribed statins. So no, cardiologists don’t always do the genetic test.

Now that I have been enlightened regarding all of the cholesterol controversy over the past few years, I am seeking out a genetic test to be sure. I’ve lived in fear because I had to stop the statin in order to start a family and the doctor told me “you better have your kids as close in age as possible and get right back on your statin”. Well, I still haven’t gone back on at this point and will not until I have more information. I have drastically changed my diet (low-carb) and managed to decrease lipoprotein a from the “very high risk” category to the “low risk” category. I was shocked by this as many online sources say there is very little one can do to lower this risk marker.

Lisa: What values for Lp(a) are considered “high risk” and “low risk?” Mine was tested 4 years ago (Quest). The reference range they list is < 75. Mine was 76, so I'm not terribly concerned. My father died of an MI at 32, but I think WWII had a lot to do with it; all of his siblings lived into the 60's and 70's, except the youngest, who is very much alive at 91. His father lived to 87, his mother almost as long. My own mother lived to 97.

Gary, I’ve seen various units of measurement out there. What was yours measured in? Mine was initially 484 mg/L (48.4 mg/dL) and is down to 191 mg/L (19.1 mg/dL) which is low according to the lab that tested it. But online it seems I’m borderline (which is in the range of 14 to 30 mg/dL). According to https://www.docsopinion.com/health-and-nutrition/lipids/lipoprotein-a/ less than 14 mg/L is ideal.

Lisa: Sorry that I neglected to give the units. I usually comment at 5:00 a.m. The units I was using were nmol/L, so my result was 30.4 in mg/dL, just above the reference range. This was a year before I gave up eating grains, so I wonder what impact that change has had. I eat meat, seafood, fruits and vegetables (some fermented), mushrooms, nuts, (100%) chocolate, cheese, cream and butter, and not much else.

“To rephrase their statement. We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him. I have an alternative, and much simpler explanation: LDL does not cause CVD. My explanation has the advantage that it fits the facts of this case perfectly, with no need to start looking for any alternative explanation.”

well said Doctor!
But, but, are your colleagues going to pat you on the back?

Thank you for this post..It is very illuminating.
Malcolm,you wrote that the authors of the paper, rephrasing… them, state. ‘We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him”.
If they are putting forward this ‘hypothesis’ they have a scientific obligation to investigate & demonstrate it.
” Quod Erat Demonstrandum” = QED !That I is what we were all taught in science at school when I was young.

Do you know of any such research ? And does it come anywhere close to understanding what ‘protective process’ is at work ?

They are, I know, looking for something/anything that could be protected this man. He has been extensively studied, and nothing has yet been found. Of course, if you study someone for long enough, you will almost certainly find something unique to them. I have suggested, to him, that the researchers look more closely at his blood clotting factors. Because FH and factor VIII are often closely linked – genetically.

Having tried long & hard & discovered zip, their ‘protecting factor’ hypothesis’ is itself scientifically untenable…’Bunk’ science !
Qod Erat Non Demonstrandum or ‘QEND’ …
This ‘QEND’ness’ must be stated to be such on any & every occasion.
There is. more blunt colloquial way of saying this here in Oz : ” Not worth a pinch of s**t”.

Am I correct in assuming that this means that people with FH have blood that more readily clots? http://www.bloodjournal.org/content/118/26/6990 Excerpt: “We demonstrated that patients with heterozygous FH had on average a significant 9% higher FVIII level than unaffected relatives. This finding confirms the hypothesis derived from previous findings, suggesting that the LDLR might have a suppressing role on FVIII levels.”

And if the levels are higher for me (I think this is me too, but I’ll head over to promethease and hope they can find it for me), then my blood might more easily clot?

Because it seems like that study/report is assuming foreknowledge of the function of FVIII and I don’t have it. And if my reading is correct, you might have just prevented a recurrence of pulmonary embolisms for me. I’ve been living in fear of that ever since it happened the first time and nobody could say why.

Let me ask, is this a Neanderthal DNA variant? because I have lots of those, and some of them also affect clotting.

Thank you as always for a thought provoking article, your insight is much appreciated.

Taking a guess….I would think it a Good Idea for a FH (diagnosed) 65 y/o male who has ditched his statins… to suggest his GP consider a Prothrombin Test ? (Clotting time)
One of the Useful Side Effects of statins being it’s influence on platelet aggregation.
– That and ‘anti-inflammatory’ being the only things I’d grant as being value in a statin…

As another black swan I enjoy reading your reports. My genetically proven FH family was and is free of CVD and reaches very high age, also never treated members with severe obesitas. After 35 years of intensive statins I saw my GTT deteriorating and found a very high CAC although no reduced coronary lumens or exertional ischaemia. I am on ketogenic style, reversed IR almost instantaneously, and switched to nonsystemic cholesterol lowering direct after finding this CAC, as I suspect statins might be a potential cause of both the IR and the CAC. I strongly feel that the single urgent stepfor all FH’s is to get out of inflammation immediately, and to question the potential damage by statins on mitochondrial health, insulin resistance and response, and K2 availability. Scientists and guideline committees should at last take their responsibilities.

Bill in Oz, Dr. Kendrick outlines some of these in one (or more?) of his books. He discusses one group of people with very low HDL yet also very low rates of heart disease.

My personal opinion regarding HDL is that it’s a marker for high carb intake/insulin resistance. For instance, I always had HDL below 40 when I was on (very) low fat, no matter how much exercise I did. It was only after going low carb (and then intermittent fasting) that my HDL went up.

The other issue with all of these is that you can manipulate them based on what you eat and how much you fast. Here are my values (all in US units, mg/dL):

From 2/29/16 to 3/4/16, I fasted 4.5 days, and you can see what happens when you do this. I transitioned to a low carb diet 1/1/14, and started intermittent fasting about 1.5 years later. The 9/18/15 test is also after 4.5 days of fasting.

My personal opinion is that it’s unlikely HDL is “protective” (especially since drugs that raised HDL were actually bad for you), but it’s a marker for something else. Higher HDL is “good” in the sense that if you reduce carbs/insulin resistance, you typically have higher HDL.

Strutting around with your high HDL value may just be a case of “pride goeth before a fall” (I admit I felt better about my high LDL when my HDL was also high).

My sense is that nobody, and I mean NOBODY, has any idea what causes CVD. That’s what makes Dr K’s long series so compelling. It addresses the problem in all its magnificent, confounding complexity. Medicine has been studying heart disease for seven decades, and medicine can’t reliably predict who will be stricken and what to do about it.

You know this points to a much bigger problem right through medicine. Once a hypothesis gets stuck in the system, you have a problem. Future research is based on it , sucking up valuable dollars and preventing anyone from imagining any new questions to ask, negative research does not refute it, authors of papers unthinkingly refer to it as prior art, thus increasing the number of hits on search engines and creating the illusion of respectsbility. Then we devise treatments on that theory and waste our patients time on it. When the field gets really big ( ie ADHD, which is the most researched condition in Medicine) specialists in the field are so overwhelmed with work in reviewing that research that they have no time for any new ideas.

ADHD is a great example as the “ dopamine hypothesis of ADHD” is a perfect e ample of this problem, which maybe should be called “ The Emperor’s Research Team have no clothes. I am intending to publish my challenge to the dopamine hypothesis, but this is too big a topic for here.

There are plenty of other examples but the commonality is an initial hypothesis of causation ( often based on a treatment found by chance to be useful) which gets carried into the mainstream and has life breathed in to it without sufficient consideration.

Overall, I think the thinking deficiencies inherent in this process may be more damaging to medical science than the low confidence intervals regarded as satisfactory or the issues of founder biassing of research.

Indeed. I find that I am increasingly interested in why people think things, rather than what they actually think. More critically, how can you get people to stop thinking the things they think. From the film Inception. ‘The most resilient parasite is an idea planted in the unconscious mind.’ I believe that we mostly allow ideas to enter our ‘unconscious/zombie’ mind without assessing them first. Ideas that ‘fit’ with our view of common sense, slip past out conscious thinking, into the unconscious mind where they merge together and grow stronger. Then they link to the Amygdala, so that they start to trigger strong positive emotions. Attack that clump of ‘common sense’ ideas, and you then trigger an aggressive defence mechanism. The trick is to attack the ideas from a completely different direction in order to outflank the unthinking defence mechanism. At least I think that is the trick.

Malcolm & Mindbody,
I suggest we need to step back a little and see the bigger picture. We are ‘human’. And a key characteristic of us humans is we naturally belong to ‘tribes’.
There are national tribes. But more important are the tribes we all belong to at the sub national levels. You grew up in Glasgow. And there in Glasgow there are two antagonistic tribes : Queens Park Rangers & Celtic…Here in Oz Australian Rules Football has the same identical phenomenon. No Collingwood supporter would ever, ever have a good word for a Melbourne club supporter. .
Folks are not in these tribes for ‘rational’ reasons. These teams are part of their sense of who they are, their identity.

Doctors, cardiologists are human and have that same instinct to be tribe members……And a key ‘belief’ in this tribe is the LDL causes cardiovascular disease…

Accepting that this is false/fake/ dumb etc. will undermine their sense of belonging.. And if they actually go public with their doubts, they will indeed become outcast from the tribe..

Only when the leaders of the tribe have changed their minds and said so publicly, will it be safe for these tribal medicine doctors to also change their minds.

When will that happen ? No answer comes to mind just now..But I think that time is close.

In the meantime it’s important that all folk who have examined the evidence, understood the reality, and seen the light stand together as a tribe and call out the fakes for what they are.

Which leads me to end up by saying, “Hey, thanks for leading this tribe !”

I think if you went to Glasgow and looked for a Queens Park Rangers supporter you may be disappointed. London may be a better bet. Also, I grew in Dunfermline, and was thus required to support Dunfermline Athletic (the Pars), which I did – and do. Even though they are a bit rubbish at the moment.

I happily accept correction on this..
After all my family left Liverpool in 1952.. And I follow AFL not soccer. So I am a bit out of date on it… And if QPR’s and Celtic have put aside some of the old animosities that I heard of as a boy, that’s all for the good !

Thanks Martin for sorting out my confusion on these soccer clubs… I confess I rarely watch soccer games at all.and am not. a fan of the game for reasons which could in expressed land me in the midst tribally based criticism… 🙂
.I was just trying to make the point with local UK examples.

I watched the film Inception (which Dr. K. quoted from) last night…. WOW!
Very intriguing ideas, and on so many levels….literally.
Complicated to watch, for me. It seems to be a film that should have been a series of about 10 episodes, but was packed into a shorter time period. It would make a great series.
Must be the most unusual movie I have ever seen, but I’ll have to watch it again to see if I can follow it better the 2nd time.
The special effects are amazing. How the heck do they do that stuff?? (rhetorical question, and sorry to be off-topic!)

This is a question that has been on my mind increasingly. I note with a small bit of horror that some of the smartest people I know are unable and unwilling to think for themselves. Most people are followers and even many leaders are followers of bigger leaders. Since I am not wired that way, it is disconcerting and even weird. Rather like being awake among sleep walkers. I do see the value in tribal coherence. I just don’t know what role nature has for the likes of me. I do like people but I am uninterested in following the crowd, nor do I play hierarchical games or vie for a leadership position.

Yes, that’s the way we humans are AnnaM.
I’ve been in a number of ‘tribes’ in my 70 years..They all claimed to be right and infallible. And so I bailed out of almost all of them when I saw their flaws and stupidities..And on. every occasion, my fellow tribal members were perplexed and confused as if I had betrayed them personally…

On the last occasion I simply tip toed away quietly with no explanation… Simpler & less stressful that way.

But I wonder, does not being a part of this electronic community, bring you some satisfaction & joy ? It does for me !

My trick has been to start out by agreeing with them, It’s always pleasant to have someone tell you you are correct, and then, like I’m sharing some deep dark secret, I ask them ….” but did you hear about ….( insert a little tidbit contrary to their belief, and yet amusing) ” , now you’ve shared something with them, this forms a tight bond.

You could also ask them for a favor, ” Could you help me review this crazy paper saying such preposterous things …”

I’ve begun to see the value in old sayings ” You can attract more flies with honey then you can with vinegar”. Vinegar being the sour attack on their emotionally held belief; you can never change their mind with a direct frontal assault, but you can lead the horse to water and hope they take the drink.

Your blog has always been a robust source of little tidbits….thanks.
Doug

Bill in Oz,
Ive often made a similar point about tribes. We are biologically evolved to want to fit in to the group- but to fit in to a group of no more than around 150 people. The penalties for crossing the group are severe- who would want an orthopaedic surgeon pointing the bone at them? This need to fit in can be, and is being, exploited by unscrupulous individuals who understand the rhetorical, and hypnotic techniques described by Edward Bernays- Freud’s cousin.

Can I use the sporting tribe metaphor again..( But I will stay away from Soccer as it’s not my strong suit. )

In Australian Rules Football sport here in Oz, the great and only aim is to win. Preferably by as many goals as possible as the bigger the winning margin, the more obvious how bad the opposition are.. So a game where a good side wins by 10-15 goals is pretty normal. ( By the way, unlike Soccer, nobody wants a draw. Draws are very rare and a disappointment. )

The aim of the game is to win by such a margin that the opposing team & supporters all go home demoralised and in no mood for a barny after the game.

What am I getting at here ?

Simple, the need to blast away the opposition tribe by scoring lots of goals… And sending them home feeling clueless, bewildered and exhausted.

After all this is exactly what the “Cholesterol hypothesis ” have been doing for decades with their game plan based on poor poor science.

Respecting them as all knowing, well intentioned & rational, medical doctors with ‘authority’ will not achieve this…

Incompetent mistreatment of people with serious CVD, is not a time for a cricket type “jolly good show type ” response.

Convinced that high cholesterol is better than low cholesterol.
Could not find any info on raising cholesterol. Here are the recommendations for lowering cholesterol. Assume that i have to do the opposite.
“To help prevent high cholesterol, you can:
Eat a low-salt diet that includes many fruits, vegetables and whole grains.
Limit the amount of animal fats and use good fats in moderation.
Lose extra pounds and maintain a healthy weight.
Quit smoking.
Exercise on most days of the week for at least 30 minutes.”

My husband – airline pilot – has FH and a reading of 12.5 . During one of his medicals ,calculus was spotted around his eyes and he was immediately put on statins . Within a week his left knee and leg had swollen so much he could not walk and had a great deal of joint pain. He asked the consultant about this and was told it could not be the statins . Having never suffered any ill health in his life ( never had a day off work ) and doing some internet research he stopped the statins , the swelling went down but then his blood pressure went up , his knee has been a constant source of pain and he suffers from Iritis . This was 10 years ago . He was told by consultant it was so unlikely to have been statins and only way to find out was if he took them again . Needless to say he ignored that . He now has to take blood pressure lowering tablets but apart from iritis that comes anD goes is in excellent health. He is very fit , has excellent diet and a happy character. As a background to this story his father is 98 with a similar high cholesterol reading . He was put on statins at 90;- no Ill effects although some signs of mild dementia – why put a 90 year old man on statins ?

Having been practicing nursing for 50 years, I have watched the “normal” levels for all sorts of lab values change according to the political correctness idea of the moment. When I graduated in 1968, a “normal” cholesterol was 220 (US). Now it’s less than 200 and still on its way down, without a shred of evidence to bolster the change.

Beth: I find it amusing (?) that for lipids and hypertension, “normal” ranges as previously presented are rapidly being replaced by “normative” ranges, so that if your lipids or blood pressures exceed recommended figures, you are flagged. So far as I can tell, though, a large percentage of “normal” people get flagged this way and they are pressured to take statins and blood pressure meds.

“To rephrase their statement. We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him. I have an alternative, and much simpler explanation: LDL does not cause CVD.”

I have a third explanation: We all know that this man is not an exception. You provided enough evidence before already. We know that there are many people with high cholesterol and faring much better than people with low cholesterol. We also know that many people with normal cholesterol levels get CVD. Cholesterol, calcium, several other substances, inflammation, oxidative stress, blood flow, genetics, stress and other factors are implicated in CVD. And I think they all work together and depending on certain “constellations” you get CVD, or not.
Scientists and doctors are always looking for causes, preferably just one, but in the case of CVD, unlike is the case with infections, I believe there are many, many causes, it’s actually a big mess. And you can single out a few “co-causes”, like for example cholesterol and CVD, but what you find will always be unsatisfying and only be part of the story.

Science is not yet ready to deal with this tangle of causes. But as artificial intelligence is emerging in the medical domain, I think the future is promising. I think artificial intelligence will be able to find links and interactions (and maybe new causes) between factors of CVD much better and easier than humans can.

Very neatly and succinctly summerized!
However, it seems to me that unless we all have nano-robots constantly crawling over and through us collecting information, AI will only be as good as the spotty and flawed information we prejudiced and flawed humans give it to work on.

“Body sensors” exist and are being developped and get always cheaper, so yes, in the future much more information on body functions can and will be collected.
Yet even now, with the information doctors themselves collect, artificial intelligence can often make more accurate diagnoses than humans.
But of course you are right: The more information collected and the less biased it is, the better AI will function.

It’s unfortunate that the medical world is hopelessly behind as to artificial intelligence. I am sure doctors could make much better decisions and provide better care for their patients if artificial intelligence would be used. There is so much knowledge out there, doctors can’t know everything – not knowing everything is not their fault, but not using/developping specialised software to always get the right information for the right patient IS their fault.
It seems a change must come from companies like Google who are developping AI for medical applications.

There is one very high quality body sensor. It is called Mind. The most effective app I have encountered for upgrading the sensitivity and specificity of that sensor is called Vipassana. It is very cheap to download, but the installation takes at least 10 days. It is not marketed by Google.

I think AI will find many, many spurious correlations, each of which will have to be checked out. For instance, did you know that there is a 99.26% correlation between the per-capita consumption of margarine and the divorce rate in Maine? You and I know there is unlikely to be a link but I’m not sure a machine would know.http://tylervigen.com/spurious-correlations

Then there’s the happy accident, a source of many medical advances. Viagra and most of the psychoactive drugs were initially intended for something else and only on trying them out was their current use found. The ‘stress causes disease’ hypothesis which Dr Kendrick promotes came about because of Hans Selye’s carelessness in handling laboratory rats. Without human intervention these are unlikely to be discovered.

It is testing hypotheses that takes the money, time, and ingenuity. AI can’t test hypotheses. It can only generate them. Maybe, by being able to encompass a wider range of data, an AI might get lucky and hit on something a human might not have noticed, but I don’t think the day will come when we can turn on the computer and sit back while it solves all of our problems.

never said AI will state and test hypotheses for us. But in this case, it may have stumbled onto something that others had found and explained before. The caveat being that both graphs had a mostly monotonous downward slope without any exciting peaks to match so it may well be pure coincidence.

A different black swan:
Those brilliant electrophysiologists in Australia headed by Dr Sanders have come up with a protocol that virtually cures atrial fibrillation. Just lose 10% or more of your body weight and there-ya-go, fixed. That would seem to indicate the cause of AF is overweight/obesity.
If I had addressed this mode of cure when in my fifties at a lean muscular BMI of 22. I’d have to have cut drastically into that muscle mass to lose that amount of weight.
Clearly, weight does not necessarily = fat.
Clearly, fat did not = AF for me.

JDPatten, re weight loss and AF.
My thinking at one time was that heart cell health would affect electrical signal generation and conductivity. A slight change in cell size could also be a factor. At this point I came across mTOR as regulator of autophagy. Clearing out cellular junk via inhibiting mTOR by reducing glucose, insulin, protein and linoleic acid (PUFA) and combined with periodic fasting (meal timing) my weight dropped 10%. Added a bunch of supplements as well. AF free now but took several years. AF triggers during that time were excess carbs or protein and strenuous activity.
Never took prescription drugs or aspirin for any condition. Maybe it is not weight loss but autophagy that can cure AF. The weight loss is a side effect.

Andy S,
I perceive that AF cause may be multi-factorial from all the stuff I have read. Certainly stress and high carbs seem to be involved. Moreover, I have read of some who have cured their AF. The question of “cure” is at what level of occasional fibrillation does it become “NOT AF”. I don’t know.
Another idea that came my way was that high carbs = leaky gut. Perhaps some of the leaked “gunk / bacteria” affected the heart = AF (perhaps). Therefore, correct diet (LCHF?) overtime allows the immune system to “fix the “gunk/bacteria” and so reduce / remove AF.

Would love to know more as to AF cause, how the cells are affected by what means, and therefore potential “cure”. Any ideas?

https://www.cell.com/cell/fulltext/S0092-8674(17)30414-2
Resident Macrophages: Near and Dear to Your Heart
“This raises the intriguing possibility that the newly identified cardiac macrophages might somehow affect morphogenesis of the cardiac conduction system and/or shape how it responds to injurious insults, such as hypoxia and infection.”

http://www.jimmunol.org/content/jimmunol/197/8/3293.full.pdf
“In conclusion, in this study we demonstrate that diabetes is different from chronic colitis and induces a systemic proin- flammatory state primarily through broadly increasing the mac- rophage population in various organ tissues. Although additional investigation is needed to further define the mechanisms, strat- egies aiming to reduce monocytosis in the spleen and limit macrophage proliferation in tissues may become important for controlling diabetic complications in conjunction with hyper- glycemia mitigation.”

I might be one of the people you are talking about. A week ago I was tested and my LDL was 369 (468 total). So far the cardiologist can’t find anything wrong with my heart though I haven’t had a calcium scan yet. Something I am worried about is my eyesight – I have amd at a young age and I have to wonder if it is from high circulating choelsterol. What about people with xanthomas? The body does appear to be trying to get rid of the stuff, that can’t be good. Maybe high cholesterol is fine but genetically high cholesterol overwhelms.

I might be one of the people you are talking about. A week ago I was tested and my LDL was 369 (468 total). So far the cardiologist can’t find anything wrong with my heart though I haven’t had a calcium scan yet. Something I am worried about is my eyesight – I have amd at a young age and I have to wonder if it is from high circulating cholesterol. What about people with xanthomas? The body does appear to be trying to get rid of the stuff, that can’t be good. Maybe high cholesterol is fine but genetically high cholesterol overwhelms.

Malcolm I have just been looking through your first source link. It bears repeating and thinking about :
1: The ‘patient’ was diagnosed with FH in his early 20’s ( at college)

2: Ever since then (>50 years) he has been prescribed a whole swag of LDL-C lowering drugs including high dose statins.
3: These prescribed drugs all completely failed to reduce his LDL-C levels to a ‘safe’ level.

4: But contrary to all expectations he has a CAC level which indicates no calcification of his arteries at all…

The authors then go on to cite the following as important in protecting him from CVD:
Not smoking
Normal BMI
Not being hypertensive
AND “eats a high-fat, low-carbohydrate diet.”
And ” possesses a strongly positive life outlook.”

I was diagnosed with high LDL levels 10 years ago. The reaction was to get all my children (then in their twenties) tested so that they could be put on statins if necessary. Alarm bells rang. I refused statins and nothing more was said. I only know my mother’s family history but there is no heart disease there back 3 generations.
Ticking the box of knee-jerk statin treatment with families of black swans is a blinkered and dangerous way to respond to evidence that doesn’t fit a faulty hypothesis.

My wife and I – now 71 and 69, have always had ‘high’ cholesterol…… and no CVD… In fact, when I had my first knee replacement some 7 years ago, and went through a raft of preliminary tests including heart monitoring – the nurse told me I was the fitest man of my age group she had seen for 6 months….. A worrying related Mail news item today – GP’s being paid to prescribe drugs, no time to monitor patients need for medication, and a whole raft of medication induced medical conditions – which miraculously disappear when patients take themselves off medication…. My GP and I have an understanding, in no small way due to your blogs on cholesterol statins etc etc… we have a partnership, an equal responsibility for my health. Too many patients pass the buck for all medical issues to their GP….. without questioning anything…..My GP knows why I will never take statins – she has a detailed letter from me on the whole Cholesterol/diet/CVD/statins issue …. as the old BGAS advert used to say…. ‘it’s good to be in control’…… Thank again for all your intelligent health wisdom

and the clot thickens… This gentleman has low Lp(a) . I told my Doctor that is the “bad” bad cholesterol. I told this same Doctor that saturated fat does not cause heart disease about 20 years ago. Thank you Dr. Kendrick.

Not sure what you mean by “amd” and I’ll be curious to see if your doctor puts you forward for a CAC scan.

I had cholesterol on one of my knuckles and this, along with high serum cholesterol, was another reason for assuming FH. I didn’t have FH.

While getting my FH genetic test done I was given plenty of literature to read including The British Heart Foundation’s booklet “Life with Familial Hypercholesterolaemia”.

Page 26 covers

(1) tendon xanthomata (with a picture of swollen knuckles) stating “it’s believed that tendon xanthomata are only found in people with FH” (not true in my case) and

(2) xanthelasmas (cholesterol deposits around the eye) stating “if you have these, it may be an indication that you have high cholesterol, but it doesn’t mean that you definitely have FH”.

The booklet doesn’t explain why these deposits occur and it could be as you say the body is trying “to get rid of the stuff”. But then why produce so much of the stuff? Unless…

…Not having FH, my problem was trying to figure out if my high cholesterol was either (1) naturally high or (2) part of ongoing arterial damage/repair process.

I’ve no idea.

The booklet also provides the Simon Broome criteria for diagnosis of FH as follows:

Definite FH is defined as follows (adults):
1. TC above 7.5 mmol/L or LDL chol above 4.9 mmol/L
plus either
2. tendon xanthomas in the patient or close relative
or
3. DNA based evidence of an altered gene

and

Possible FH is defined as follows (adults):
1.TC above 7.5 mmol/L or LDL chol above 4.9 mmol/L
plus either
2. family history of heart attack below the age of 50 in second degree relatives (e.g. grandparent) or below age 60 in first degree relative (e.g. brother)
or
3. family history of raised cholesterol.

The diet is the most important thing to ask about. Low-carb with natural fat (no vegetable oil or shortening) is what gave me a zero plaque diagnosis. The cardiologist was amazed to see such a sonogram in someone my age, but he never asked me about how I got it. If he had, I could have told him. He still tried to put my husband, who eats a similar diet, on statins!

I guess that I am a black swan but at the other end of the cholesterol spectrum.

At my serious MI 1999 they measured so low cholesterol levels that they didn’t think it was worthwhile to put me on statins – lucky me!. With my life style changes I then introduced all lipid measurements still improved; lower TG, lower LDL and higher HDL. Although I didn’t take any of the prescribed medicines I was patted on my back and encouraged to continue with “whatever I was up to”.

I appreciate Dr Malcolm Kendrick’s viewpoint very much and I respect the man very much. I am an American physician who has passed the National Lipid Association Certification test and many years of treating patients with risk factors or + CAC to target LDLc < 70 or non-HDLc < 80 and LDLp < 750. I asked Doc Ken if much of these cases with high LDLc and high HDLc can be understood better with the biomarker Non-HDL cholesterol or LDLp? In your cases what is the non-HDLc? LDLc is a very poor biomarker especially because of discordance if Triglycerides are high. I always appreciate your viewpoint but wish you would include biomarkers non-HDLc or particle counts such as Apo B. Thanks

Thanks for you comment. I may do in future. However, my general view is that all of the ‘splinterings’ of the LDL hypothesis are simply an attempt to retro-fit the facts to fit the hypothesis. What some would call adaptations, or the creation of ad-hoc hypotheses. As another general view I believe LDL, in whatever form it is measured, to be (mostly) benign. Low HDL and raised VLDL is a sign of underlying insulin resistance [though I do not like this term] and this combination is relatively pro-atherogenic, primarily though impacts on blood clotting. Obviously, it is more complicated than that.

Brain, while Dr Kendrick may thank you for your comment. I do not.
Iid a quick count and of the 118 words in your comment 21 of them are highly technical and jargonistic…
And I notice that you think it’s important to claim ’eminence’ & authority bu citing your quals.
Bugger me ! The only way to earn my respect is knowing whether your patients with Cardio Vascular Disease are ‘cured’ via your treatment…

AHN, I do not make any claim to being a medical doctor or authority in medical science. But my criteria for assessing them is the same as for most other aspects of life : “Does What They Do Work ? ”
If what they do does not work, then their claims for eminence and money are bull & not worth respecting….

On the other hand I notice that lots of folks still operate on the old class bound status way of thinking…And take disrespect as a threat to the stability of society…

Note his rationale to test for a condition which he initially says is UN-treatable, – then rabbits on
in Detail with his……. ‘Treatment’ protocol. !
Would be cheaper to just go with Vitamin C, proline, lysine and maybe Vit B3 for good measure.

Thanks for the link, Janet. It is a fascinating example of the dissonance surrounding CVD and lipid levels. I too was struck by the idea that Lp(a) appears to be a marker for CVD risk, yet lowering it does not appear to be of any benefit.

I don’t know if you clicked on the link he provided, but this was interesting too –

This doctor states “Dietary changes, exercise, and weight loss have not been shown to lower Lp (a).” Then two paragraphs later: “One study documented a lowering of plasma Lp(a) levels in individuals placed on diets rich in saturated fat (a palm oil enriched diet). In keeping with this, other investigators have reported an increase in Lp(a) levels in individuals after they reduced their saturated fat intake. Monounsaturated fats also seem to reduce Lp(a) levels, as shown by a study that reported a significant decrease in Lp(a) levels in individuals whose diets were supplemented with almonds.”

At which point, my brain said something like, Er, what?

And then he noted this, “Niacin lowers Lp(a) by approximately 30 percent. Therefore, the EAS Consensus Panel has recommended niacin as the primary treatment for lowering elevated Lp(a) levels. However, these recommendations may have to be reevaluated in light of the results from the recent AIM-HIGH and HPS2-THRIVE trials. These trials did not show any clinical benefits of adding niacin to statin therapy.”

KidPsych, I have been doing exactly this for the past year..No statins at all but taking Niacin as part of my own treatment plan…But nobody is interested in testing to see if it ha worked…

By the way Janet, Niacin is getting harder to find here in Oz and it has gone up in price about 200% this past year…It is certainly far more expensive for me than any statin. But then the Australian Medicare system subsidises the statin prescriptions but not Niacin…

It is essentially an advert for genetic testing for FH. There is a graph about 1/3 into the presentation that I don’t get. It shows the distribution of LDL in non-carriers and carriers of FH mutations. Aged 45-54, the average for non-carriers is 3.1 vs 4.6 mMol/l for carriers.

That means the non-carriers are well below the general population average, and even the carriers are slightly. What’s going on here?

What his bilirubin levels are? Bilirubin is a powerful antioxidant. I have noticed that TH and LDL fluctuations always go with corresponding bilirubin fluctuations. Any studies on that? I am a female 106 lb with the latest TH 314 and 211 LDL, up from the “usual” upper 200s and 100s. HDL is good. Bilirubin had always fluctuated correspondingly. Negative for FH type 1. Out of seven genes that are most responsible for LDL levels, the #1 in my case is normal. My thoughts are that bilirubin plays some important role in keeping a person’s heart with high cholesterol healthy. My mother 81 has high cholesterol and no heart disease. I couldn’t find any studies on cholesterol/bilirubin relationship in people who have both always elevated from what is considered normal.

The problem is that there is very little root cause analysis going on. High cholesterol for genetic reasons with no other underlying cause is completely different from high cholesterol which coincides with insulin resistance. In that case, the high cholesterol has an underlying cause which is itself the reason for atherosclerosis, not least by inflaming the arteries, which the cholesterol attempts to heal.

brwims, particle number re. cholesterol testing seems to have merit. A few huge ldl particles better than many small ones at same cholesterol level. Something about a fatty liver attempting to export excess triglycerides. TG:HDL ratio is an indication of what is happening. Root cause is too many carbs ending up as fat droplets in the liver.

FTL: The results of the analysis revealed that there was a significant correlation in all the women between the diversity of the microbes in the gut and the health of the arteries. After adjusting for metabolic variations and blood pressure, the measure of arterial stiffness was higher in women with lower diversity of healthy bacteria in the gut. The research also identified specific microbes which were linked to a lower risk of arterial stiffening. These microbes have also previously been associated with a lower risk of obesity.

KidPsych: Thanks. It has become abundantly clear that this long-unknown organ-the gut microbiome-is a powerful and crucial modulator of overall health and brain function and health. The relationship of its inflammation with neuro-inflammation, commonly called ASD, is now firmly established in the literature. Time for Richard Horton to re-instate Wakefield, et al. His own words bemoan the rarity of replication, yet the key findings of this paper have been repeatedly replicated by those who’ve managed to get some funding.

A new national study has shown that nearly75 percent of patients hospitalized for a heart attack had cholesterol levels thatwould indicate they were not at high risk fora cardiovascular event, based oncurrent national cholesterol guidelines.

Specifically, these patients had low-density lipoprotein (LDL) cholesterol levels that met current guidelines, and close to half had LDL levels classified in guidelines as optimal (less than 100 mg/dL).

“Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk in most who could benefit,” said Dr. Gregg C. Fonarow, Eliot Corday, Professor of Cardiovascular Medicine and Science at the David Geffen School of Medicine at UCLA and the study’s principal investigator.

“The study was sponsored by the Get with the Guidelines program, which is supported by the American Heart Association in part through an unrestricted education grant from the Merck Schering Plough Partnership.
Fonarow has conducted research for GlaxoSmithKline and Pfizer and serves a consultant and has received honorarium from Abbott, AstraZeneca, GlaxoSmithKline, Merck, Pfizer and Schering Plough companies. He is also chair of the Get with the Guidelines steering committee.”

That’s an interesting point you make above. I had considered the tribal element of safety in staying with the group, but I had not thought of fear of group anger or rejection as a motivator against thinking for oneself.

AnnaM, thinking outside the box (tribe) could be a sign of maturity.
ttp://www.psysr.org/about/pubs_resources/groupthink%20overview.htm

“Groupthink, a term coined by social psychologist Irving Janis (1972), occurs when a group makes faulty decisions because group pressures lead to a deterioration of “mental efficiency, reality testing, and moral judgment” (p. 9). Groups affected by groupthink ignore alternatives and tend to take irrational actions that dehumanize other groups. A group is especially vulnerable to groupthink when its members are similar in background, when the group is insulated from outside opinions, and when there are no clear rules for decision making.”

I have a number of patients with high cholesterol and a coronary artery calcium score of 0
A 93 year-old with total cholesterol was given statins but stopped very quickly as she felt very ill.
There seems to be a gentle lessening of the cardiologists fanaticism about cholesterol, so maybe they are listening to people like Aseem Malhotra. At least he is a cardiologist, I am just a GP.
Conversely I have written in black white, something which I regard as the ultimately brainwashed cardiologist’s response .”Angiogram completely negative in a 65 year-old lady, no sign of any plaque formation, no visible stenosis in any of the coronary arteries. Treatment plan-Lipitor 40mg”
There is a complete lack of common sense in the medical profession.

Indeed there is. But medicine relies, to a large extent, on conventional thinking to work. Gaining group agreement for various medical activities makes everyone, including the patients, feel highly reassured. ‘This is the correct treatment for you, it will work etc. etc.’ The problem is how do you then move from doing A, to informing the patient that ‘actually A is nonsense, we now need to do B,’ without destroying the necessary comforting authority at the same time?

Perhaps we just need to get the sheep to start chanting. ‘Four legs good, two legs better.’ And hope for the best.

Which, Dr Kendrick, lets the cat out of the bag, this feline being The Placebo Effect.
Suddenly doing an about-face like that could devastate the patient… and we all know about the ORBITA study proving ‘Faith’ is as effective on physical performance as…. a stent…
Ooops.

It’s worse! Here in the US, a cardiologist who fails to push statins on patients with high cholesterol has a good chance, if said patient suffers a heart attack, of a lawsuit (with Fonarow testifying for the plaintiff?). I rather doubt I can find a “credentialed” cardiologist here in southern California who doesn’t preach the AHA party line. Rather recently, my UCLA cardiologist pretty much refused me as a patient since I reject statins…

But Tim, if your hypothetical patient refuses statins from the indocctrinated cardiologist and seeks out actual helpful advice on how to minimise the rick of a heart attack, there is a very high risk of being ‘cured’ !

Unfortunately such a patient would thereby lose the opportunity or no need to sue..

Ohhhh wow, such a choice ! Me oh my, what to do ?

Well I know what my choice would be..In fact I made exactly that choice !

As for your hypothetical cardiologist ? Well if all cardiologist patients took this course of action, as a profession they would either quickly out of business or they would change their ideology very quickly..

When discharged after an MI, I was handed a goody bag of medications: statins, anti platelet aggregation, aspirin, beta blockers, and the all important PPI, because “I’ve never had a patient not have a hole in their stomach if they didn’t take PPIs”. And my angiogram showed no occlusion!

Yes, they have the clout yet you GPS are generalists. You have the opportunity to see the wider picture. Specialists, having a narrower field, are often lacking in this, despite the awe the public holds them in. They may have the clout but I would rather listen to you.

MGJ I’m sure that this line of thought is interesting to you… And being honest it is of some interest to me.

I am quite sure the is a good deal of scientific fraud and that some of it goes undetected….Or perhaps ‘protected’.

However this issue is here a major distraction from the topic and the task of discussing that topic. Now is not the time to be wandering off into an analysis of a 100 page opinion piece.

The task at hand noe is CVD, it’s real causes and why so many in the medical profession accept & believe false dogma about the causes of CVD, to such an extent that many many people are harmed, and even killed by the treatments authorised by this false dogma…

We all know what a ‘sect’ is. And most of us can recognize zealots when we meet them. WE need now to recognise a zealot of false medical dogma even though they are ‘blessed’ with official recognition and awarded the title ‘Doctor’

I have used religious terminology in this comment – a change from my earlier sporting ones.
But my intent is the same.

“The task at hand noe is CVD, it’s real causes and why so many in the medical profession accept & believe false dogma about the causes of CVD, to such an extent that many many people are harmed, and even killed by the treatments authorised by this false dogma… ”

Surely the answer is obvious – corrupted science produces whatever answer is most convenient – be it a wrong explanation for CVD, or a false indication of global warming. In my opinion there is value in comparing with other areas of science, because people believe scientists are always scrupulously honest, and they aren’t.

It would help a lot if mechanisms were put in place to keep science more honest – for example whistle blowers should be listened to and their careers protected. It might also help if working scientists didn’t also run public campaigns, because once they stick their necks out in public, maybe they try yo bury evidence that points in another direction.

David as it happens I agree with you on this. There is a wider problem with scientific ‘research’.It is frequently presented as the newly discovered ‘truth’ to be accepted by all at the risk of being thought a heretic.

However this particular issue in medicine is an urgent one damaging many many people across the planet needlessly.

So I see a need to stay focused rather than also embracing here a discussion of the big, wider problem.

Obviously neither of us would want this forum to swing over to extensively discussing climate change, and I trust Malcolm would do something about it if it did!

However, I think a sprinkling of references to other areas of science with similar problems, helps the case against medical science no end. I would guess some people come here without ever having doubted the validity of the scientific process in general. Seeing there is a pattern is important, because it is a scary thing to deliberately go against medical advice, to discard your statins and maybe start eating HFLC!

David, it’s been hijacked by a strongly motivated minority… and the majority cannot / will not discern the damage, much less DO anything.
That’s why it’s useful to compare sloppy thinking in different fields.
It changes how I will interact with my new cardiologist and the answers he gives me. If he’s discomforted – it will be the fault of everyone here !

Dr K obviously takes this seriously, as his book “Doctoring Data” exposes the sloppy, lazy and… Deceptive … science leading us up the garden path.

When a teenage shepherd accepted the challenge of mortal combat he did so because he saw through the same bluster which terrified whole populations.
An immobile and arrogant Goliath stood no chance against a sniper 20 metres away.
– He just couldn’t see it…

I came across that article some time back. Although I think it is good, it got rather too hung up on statistical problems. I wanted to add:

Science is rarely done in a way that avoids financial bias. The influence of Big Pharma is obvious, but NASA gets a lot of money out of supposed climate change, and in many other areas, new theories attract money to institutions , whereas retracting faulty ones possibly repel money!

People are far too ready to take ridiculously noisy/corrupted data sets, and use a computer to ‘clean them up’ so as to extract a signal of interest. It might help if they had to justify such research ahead of time, and put some lower limits on the size of any signal, below which they would not consider it to be real. This is not so much a statistical issue as an issue of common sense. For example, imagine taking a set of temperature measurements at a particular location and ‘correcting’ them for the fact that the place in question has become urbanised over time before using the results to a tiny fraction of a degree! You couldn’t make it up!

“For example, imagine taking a set of temperature measurements at a particular location and ‘correcting’ them for the fact that the place in question has become urbanised over time before using the results to a tiny fraction of a degree!”

I’m still waiting for them to manipulate any temperature data in a direction which DOESN’T conform to their pre-formed conclusions. If they ever do then I’m sure we’ll never hear the last of it. Meanwhile the medieval warm period and little ice age have mysteriously vanished!

MGJ: I find it very interesting to look at my family tree. Both my Scottish and English ancestors emigrated to the colonies in the 17th Century, the time of the Little Ice Age, also known as the Maunder Minimum because there were very few sunspots during an approximately 70-year period. This was a time of crop failures and much privation, especially in Northern Europe. This changed history. Many emigrated. Sunspots are intense storms which increase the radiation emitted by the sun, warming the Earth a bit more than it would without them. From what I read, we appear to be in or entering a period of minimal sunspots, thus we may be in for a bit of global cooling. Yikes!

Even if they actually tried to be honest, how do you get a computer to correct for UHI when every circumstance will obviously be unique. For example, Anthony Watts found an instance where one of those weather stations ended up located near to a runway!

They would need to model the circumstances of each weather station to even try to get a decent estimate.

The Bad Science of Global Warming is doing just that, especially those who peddle ‘inconvenient truth$’
– I recall a figure of a few hundred trillion as the cost of Paris Accord, – to delay Global Warming.
By Four years.

Weather station recordings need to be brought to a common baseline to be used in climate models. For instance, if an area has urbanised, the “heat island” effect would push the temperature readings higher than normal, thus falsely promoting global warming. So they have to reduce the readings.

An interesting example of the lengths to which the scientists go to get good long-term data is sea surface temperature measurements, which are very sparse for the pre-satellite days.

Marine temperature readings were taken by ships and noted in the logs. Before WWII the Royal Navy was in charge of the effort, but during the war they had other concerns and the American navy took over temperature recording duties. A researcher going through the old log-books noticed that American temperature readings seemed to be a little higher than British readings and wondered why. It turned out to be the way temperatures were measured.

From the days of sail, the British would drop a bucket on a rope over the rail and haul up a pail of seawater and measure the temperature of the water as the bucket was standing on the deck. The Americans, who started with a motorised navy, attached the thermometer to the engine cooling water inlet pipe and measured the temperature there.

There was a slight drop in temperature as the bucket was raised in the breeze of the British ships’ passage, but a slight increase in temperature of water swirling into the American ships’ inlet ports. Once this was understood, the readings could be corrected and brought to a single global standard.

Interesting article though perhaps being a too big elephant in the room?

I have just finished my reading a very “scary” but very well researched and referenced book by Heather Pringle. “The Master Plan. Himmler’s Scholars and the Holocaust”

What surprised Pringle at the end of her research was that the scholars involved were almost totally unable to recognize the obvious flaws of their basic tenets about races. A parallell to what we see among the scholars of the “statin community”?

Those that know me know that I am as anti statin and cholesterol hypothesis as they come but Dr K your post got me thinking….we know smoking causes lung cancer but not all those who smoke get it. Now I am struggling with the black swan concept. Help!

Hi Dr. Kendrick,
I just can’t help adding my own case history to this “anecdote” 🙂 I think it (i.e. mine) is a fascinating one, and worthy of the attention of some serious researchers. I believe I understand my own rare medical case well, having studied it for most of a decade now, after self-diagnosing (initially — since confirmed by specialists) two genetic conditions.
I am a monogenic diabetic (HNF1-alpha), but more importantly I have CVID. My particular case of the primary immunodefiency (PI) has been tested at Einstein Medical College, showing that I have absolutely no B-cell function (i.e. no antibody selectivity whatsoever) — zero antiody titers across the board, both at baseline (prior to Pneumovax-23 challenge) and 6 weeks after test vaccination. This is not unheard of in CVID, and indeed there are a few case studies of it, but it is rare. I believe it is always caused by early failure of differentiation of the B cells. I also have some other congenital abnormalities, such as medullary sponse kidneys (both).
Meanwhile, I have demo’d (working with Linda Hemphill at Mass. Gen. Hosp. at the time) that my LDL-c is reduced by more than 50% merely by eliminating my normal diet of cholesterol-rich foods (eggs and liver, primarily). My typical LDL-c is ~300mg/dL. It can reach ~350mg/dL at times for no apparent reason. When in the throes of a flu (my biggest remaining infectious susceptibility) episode, it will be reduced down to 200mg/dL or so.
After discovering my diabetes I made a quid quo pro with my GP at the time (also the reason I saw Dr. Hemphill briefly) to take a statin for a few months. I actually took two different ones, and these lowered my LDL-c by more than half (to ~160mg/dL), with almost identical results to dietary restriction of rich-cholesterol foods. I had a dangerous allergic reaction to simvastatin, first expoding in hives and within a few days later developing what I think could be called angioedema (gross swelling of throat and tongue, restricting breathing). I had no intention of continuing with statins or really any other lipid-lowering drug in the first place, and that was the end of it.
To make a very complex story short, my entire life’s history has been a gradual adaptation (upregulation) of innate immune function to compensate for my PI. I was a basket case in early decades, suffering constant bacterial infections and opportunistic viral infections. Now I am essentially incapable of systemic bacterial infection under ANY circumstances, and only get the flu (much more than a normal immune-competent person of my age).
Your colleague Uffe Ravnskov is well aware of the long history of study of the unusually powerful innate-immune function of HUMAN LDL. There is an increasing focus of study at the molecular level in current research by many groups, including some at UCSF who seem to favor the term “host defense”, by which they mean innate immune function. A lot of this involves hepatic response to portal cytokines, which upregulate (V)LDL generation in liver.
I suspect my LDL-c would have been normal if tested when I was young. I have as many as a dozen rare biomarkers that I can all tie to the upregulation of innate immune function. It is too much to get into in the already long comment.
My case of CVID is very rare in that I am almost 60 years of age and still immune-stable without Ig infusions (as a PI specialist would say) — this is virtually unheard of. I am convinced that my innate immune adaptation has only been possible because I have NO SIGNALING whatsoever from B cells (to the rest of the lymphocytes and immune system) — this has allowed for the gradual increase (and decrease) in expression of those (possibly ancient, from evolutionary times before auto immune system development) various genes as necessary. Efforts by the NY-based PI and diabetes specialists several years ago to start me on Ig infusions failed due to my immune stability and lack of their ability to qualify me for private insurance coverage. Just as well for me, in retrospect.
In 2012 I had a CT for coronary calcium score — it was zero, as I expected. I was fighting then, as I had been for years and years, with my GP about my LDL-c. I just wanted to prove a point, but it was of no use in the end anyway.
Anyway, I would be very pleased to be connected with any serious medical researchers interested in studying my medical case in detail. I have a lot of data to show. I believe I understand my own unique interactions, and they would go a long way toward elucidating human physiology, although in many very politcally incorrect ways. Within the limitations of clinically available automated commercial testing I have done what I can to test my hypotheses, and have not seen anything but consistent (with the theories) results.
Can you suggest any potentially interested researchers?
By the way, I have very high oxLDL (tested by Shiel Labs at insistence of diabetologist). This is just one of the many traits that I connect to highly upregulated innate immune function. With the selectivity of humoral autoimmune function, my constant immune activity is like a sledgehammer — it keeps me healthy, but not with normal efficiency. LDL play a big role, and of course those lipoproteins involved in “host defense” get oxidized in the mallay. Does that make sense?
You are one of the only bloggers that I follow, all of which I admire, that seems to think the oxLDL theory is nonsense. I myself have studied the serious experimental and observational research papers on this, and they seem remarkably and uniformly inconsistent. I decided many years ago that the oxLDL theory was completely unsupported. It is also instructive that there are almost no commerically available tests for oxLDL — Shiel Labs was the only one in the USA several years ago I believe, and they did not seem to have much demand for this test either, apparently easily handling that for the entire country.
I have abnormally high insulin sensitivity, which is universal in HNF MODY. This conserved genetic type seems to come from Nordic regions, if one looks at the epidemiology. I believe it is due to the total lack of plant foods in the diet of relatively modern humans (say, in last few tens of thousands of years) that survived in, and adapted to, these regions. There is less need for insulin, and more for insulin sensitivity, in such an environment.
In any case, low insulin/anabolism and high glucagon/catabolism are both protective against CVD in my opinion (although prandial hyperglycemia must be avoided — I use insulin to drive the excessive HGP into peripheral tissues). My physiological traits are robust with respect to CV function, and always have been. Do I qualify as another “anecdote”?

Sure … please take your time. I would sincerely be interested in connecting with any possibly interested researchers.
On reviewing another poorly written sentence of mine, I meant that I find all of the oxLDL study results to be inconsistent with the theory that it is a risk for CVD — not that the studies are inconsistent with each other 🙂
Grunfeld and Feinman are two of the Univ. of Calif. San Francisco researchers who have been studying lipoprotein immune function for decades, by the way.

P.S. I just happened to run into a guy climbing Mt. Monadnock in NH. We were both well off the beaten tracks at the time. He was a local, and an interesting character. He had been diagnosed with T2DM, in recent years. He also had an LDL-c of ~550mg/dL (that’s right, not even total cholesterol, but LDL-c). Nothing could perturb this number, apparently. He had a bad reaction to statins, I believe, and almost instantly rejected them (like myself).
Anyway, unlike myself, I suspect this guy was FH. He was in his late sixties at the time, and in very good physical health generally as far as I could tell. I discussed with him what I knew about diabetes and its underlying causes, proper therapy, etc. He was very well educated, and had gone through medical school but decided he did not want to be a doctor in the end.
He was pretty nonchalant about his LDL-c numbers. I liked that. He was, quite appropriately, more interested in discussing the diabetes.
Just another anecdote.

“We have identified a main function of nitric oxide in cellular systems,” Stamler said.

“Our work shows that the main receptors in the heart that respond to drugs don’t work without nitric oxide,” said Jonathan Stamler, MD, senior author of the new study, Robert and Sylvia Reitman professor of medicine at Case Western Reserve University School of Medicine and president of the Harrington Discovery Institute at University Hospitals Cleveland Medical Center. “The study provides new motivation to replace nitric oxide during heart failure.”

The new study, published in Molecular Cell, focuses on one of the most common drug targets in modern medicine: GPCRs, short for G protein-coupled receptors. The receptors sit on cell surfaces and are targets for nearly one-third of FDA-approved medications. When drugs like beta blockers attach to GPCRs, they influence protein pathways inside the cells. One pathway activates “G proteins” that are of therapeutic benefit, while a second pathway activates proteins called arrestins that can lead to side effects. The new study shows nitric oxide helps determine that the right pathway gets activated.

Previous studies have shown evidence of “biased” signaling inside cells, where one pathway becomes more active than another. This led Stamler and colleagues to look for natural mechanisms inside cells that could be leveraged to maintain the desired balance.

“Drugs and hormones inevitably regulate both pathways, but if one could shut down the pathway producing side effects, drugs would work better. In the new study, we have discovered how nature signals without side effects. It is able to use nitric oxide to shut down arrestin-based pathways causing side effects,” he said.

The researchers investigated nitric oxide due the molecule’s established role in receiving signals from GPCRs. The team genetically engineered mice to lack the ability to attach nitric oxide to one half of the pathway — the arrestin proteins that can trigger side effects.

“The mice had classic features of heart failure,” Stamler said. “Without nitric oxide signaling, they could not increase heart rate or pump function.” The researchers confirmed their findings in human tissue samples, collected from hearts involved in transplants. In nearly two-thirds of failing heart samples, the researchers found that nitric oxide determined signaling balance to the arrestin pathway. Many hearts showed evidence of nitric oxide deficiency (arrestin activation).

The results suggest heart failure severity could vary based on nitric oxide levels in the body. Low levels could cause GPCRs to primarily activate the arrestin side of their signaling pathways — leaving out the other half that helps the heart respond to stressors. “Without nitric oxide, heart rate and contractility can’t increase, and thus hearts fail,” Stamler said.

With hundreds of GPCRs in the body, the findings could be universally applied. According to the authors, managing nitric oxide could help existing drugs of all types work with fewer side effects. “We have identified a main function of nitric oxide in cellular systems,” Stamler said. “It likely regulates GPCR signaling across virtually all cell types and tissues. This may bear directly on numerous diseases as well as the predicted response to therapeutic agents.”

Story Source:

Materials provided by Case Western Reserve University. Note: Content may be edited for style and length.

Yes, completely obfuscating ! And completely useless as a result. I wonder if this research is publicly funded. And I wonder if any of the authors actually speak this Sciglish when they are not ‘at work’.. I suspect they do.

The whole idea of ‘Jargon’ is to exclude the Great Unwashed from understanding communications between the Annointed Ones, their Clubs, Societies and Tribes.

Being Old-Fashioned, I insist that ‘Doctors’ first live up to their title… and discharge that responsibility… before they demand the Glory Laud & Honour such honour(s) imply is their due…
– From the Latin, docere;- to teach, to show, to cause to know. The connection to ‘medicine’ and the healing arts is a later one.
If it cannot be explained in the Common Tongue, then the ‘Professor’ does not sufficiently understand what he (or she) is saying…

Mr Chris, re S-nitrosilation
Illustrates complexity of biological systems, new discoveries made every day. Nitrosilation like glycation is what happens when there is too much of a good thing like in metabolic syndrome. Illustrates that a good molecule (NO) can turn bad under stressful situations.

Dr. Kendrick, you said that some people with FH also have more clotting and they are the ones who get CVD. Are those two things even related? That is, does the FH cause the excess blood clotting? Or is it just that people with FH have been tested more extensively to find such a thing?

The gene locus for the LDL receptor also, often, incorporates blood clotting factors e.g. factors VIII and Von Willebrand Factor. In many of those with FH, there is also an increased blood clotting tendency. Thus, relatives of those with FH, who do not have high LDL, often have increased risk of CVD, through the blood clotting genes.

Not that complicated really. Let us say that you can inherit two (closely related genes). One that makes your LDL go up (A), the other that makes your clotting factors go up (B). If you have (A) you will have raised LDL levels, but no increase in CVD. If you have (B) you will not have raised LDL levels, but you will have an increased risk of CVD. If you have (A) + (B), you will have both raised LDL levels and an increased risk of CVD.

Mainstream researchers decided that this means if you have (A), this causes CVD.

My own interpretation is that this means if you have (B), this causes CVD.

Dr. K. I find comfort in the concept that genes have to be “expressed” or activated by signalling molecules to perform a function. This implies that a “bad gene” theory as a root cause of a disease is incomplete. Have to find what initiates the signal. Epigenetic factors is the first place to look I believe. The answer might be as simple as eat this or don’t eat that.

They are related. Those with FH and clotting abnormalities have an increased risk of CVD, those with FH and no (significant) clotting abnormalities do not. Relatives of people with FH ,who do not have FH, but have the related clotting abnormalities have an increased risk of CVD. I have co-authored a paper on this that should be coming out soon(ish)

I practice this today but I ridiculed it before my MI – trusted the assertions of a safe environment from our authorities!

Today more fuel was though put on “my” fire by the newsletter from Dr. Mercola regarding the agricultural pesticides and especially the ubiquitous glyphosate which is present in almost all food we eat today although the WHO has classified it as a probable(?) carcinogenic. Facts usually brushed under the carpet by MSM.

I would argue we do not need pesticides of any sort. They are just a convenient way of destroying organisms which don’t suit people at the time. The remt of agriculture is to destroy everything, except what you are trying to produce. This is a totally un-natural state of affairs. Nature works on multi-culutres, not mono-cultures. If we get rid of all pesticides, and all pharma drugs while we are about it, we could have a much reduced population, and so there would be more for those who survive.

It has been proven by serious research, as far as I understand this, that alternativ agriculture without pesticides is quite possible but you you need to understand the basic soil biology and the importance of biodiversity.

E.g., the scientific journalist Kristin Ohlson has done good digging here and written a revealing book about her findings

Goran, glyphosphate kills the fungi in the soil and so destroys soil fertility…That is why many conventional broad acre crop farmers here in Oz put out a spray of water diluted mycorhizal solution, after spraying their fields with Roundup… It is an necessary part of No Till crop farming…

Bill, would that be something like “Best TM”. ? A friend uses it on his farm with spectacular results. Not only crop growth, but stock too, as we saw during Artificial Insemination procedure recently. Vet was impressed with consistently high (internal) health of the animals. We see it as resulting from better soil condition feeding the grass which better feeds the sheep. Killing soil then eating the chemical residues is not doing our arteries any favours!

Janet, I have never heard of “Best TM” farm practices… And I have not practised No Till farming myself just studied it and watched other comventional farmers do it..

In original No Till crop farming, the farmer will spray a couple of weeks before seeding to kill all the weeds and unwanted plants in the paddock…But nowadays many spray & seed in the same pass through the field…As the seed is buried 5-8 cms. in the soil and dormant, it is not affected by the Roundup.. But the soil micro-organisms do die and there is a loss of fertility..Which is wht many No Till farmers then spray again with diluted mycorhyza brew solution…

Bill, my misdirection. ‘Best’ is a noun, name of company, and TM is the liquid product which is a pre/probiotic in that it stimulates soil flora & fauna health, – which in turn benefits the plants and the animals that eat said plants. Really simple concept and at odds with chemical -controlled agriculture.
Net result is ‘more’ nutrition all round.
Whether we eat sheep … or the plants grown in such soils, we benefit on every level.
It is my pet theory that part of junk foods’ appeal is our instinctive quest for ‘natural health’ a desire not wholly fulfilled by nutrient-poor agriculture. This same basic instinct is driving heretics such as ourselves to be dissatisfied with modern medicine and returning to sound foundations rather than propping up the leaning tower with chemicals and doubtful interventions.

Janet, Thanks for the clarification about “Best TM”… Yes a brew like that is good for restoring the micro organisms in the soil we need to grow our food; for we are indeed what we eat..

I dis similar soil ‘innoculation’ when I was farming organically…And here at home in the gardens when I started the gardens here.. But if pesticides & herbicides are not used the micro-organisms & micro-flora in the soil are capable of looking after themselves…

And I wonder sometimes : I am pretty sure there s a ink between the soil micro-organisms we grow our food in & our gut micro-biome…If one is good so is the other…I suspect..And that definitely is better for our health..

David Bailey, Roundup will reduce the population by chemical neutering, then evolution will come to the rescue with roundup ready humans. No need to starve for lack of soybeans , corn and wheat. A mini ice age could speed things up.

David Bailey, Why is such a high population desirable? Why is the goal to support an ever increasing population? It is not sustainable, particularly since the planet’s resources won’t allow it. Like every other species, the population will decline at some point. Either war (seems very close now) or a disease that wipes out most. Rabbits in the UK were reduced by 90% when myximatosis was introduced. Pesticides just poison everything else as well as humans. There are frequent cases of high levels of pesticides being found in food. It’s quite likely that is not a healthy situation, particularly in the long term. Pesticides have damaged wildlife to a wider extent than just the target. You can tell that by the diversity that exists on organic farms once pesticides are no longer used, when they are compared to “conventional” farms. Once a few more pollinating speces are removed, we might find a food shortage, and the species were removed by pesticides, so your point that the population will reduce without pesticides, will come to pass, even with pesticides.

You wrote: “David Bailey, Why is such a high population desirable? Why is the goal to support an ever increasing population? It is not sustainable, particularly since the planet’s resources won’t allow it. Like every other species, the population will decline at some point.”

I totally agree! Ideally we will continue to produce enough to feed everyone while somehow persuading people to have far fewer kids.

I spoke to a Tesco store mananager and said selling “Resolver” was a contradiction to Tesco’s claim to e selling healthy products (I know, that’s false on so many fronts). The moved it to the back of the entrance instead of it being in eyesight when you enter.

Unfortunately, glyphosate is being used in Europe, as well as Canada and The US, on more and more grains and seeds as a desiccant prior to harvest – from wheat to sugarcane. This is why it is showing up regularly in the urine of Europeans.

AnnaM: Terrible problem in Mexico, too, and many other places. Only a relatively modest percentage of the stuff is used in the U.S. A majority of Europeans have detectable levels in their urine. The National Toxicology Program has been testing Roundup (it is up for its 15 year re-licensing), and found it far more toxic than glyphosate alone. You can be certain this will make no difference in the licensing process, and that it won’t appear in the mainstream press. Trump is easily led, just like Obama, Dubya, Clinton, etc., ad nauseum. Monsanto is much too powerful, especially since it is now owned by Bayer, once a unit of I. G. Farben. Anyone remember the Nuremberg trials?

Gary, Correct me if I’m wrong… The Nurembourg Trials’ important contribution to jurisprudence was in anchoring the principle of INFORMED Consent, to medical procedures and drugs etc.
Complacency, misplaced trust and ‘amnesia’ permits Big Business & Govt. to medicate the masses and dissect the disempowered. – think accepted surgeries in recent Times, ORBITA Study for example… Pre-frontal lobotomies (“Icepick Lobotomy”) and large intestine removal, as examples of ‘Avarice- based Medicine’

Janet: Yes, indeed, the principle of informed consent was established from the Nuremburg trials of Nazi’s accused of unethical medical experimentation. Unfortunately, this principle is not a part of established law in the U.S. Three U.S. states (West Virginia, Mississippi, and California) have taken it away entirely and force medical treatment on the entire population. They’ve started with the children, but you can bet the ultimate goal is everyone. Rebellion will occur before this ever happens, but they have dollar signs gleaming in their eyes. One could argue that, despite the immense suffering in WWII, the Nazi’s actually won. Some did emigrate to New Jersey to found pharmaceutical firms. However, there was a second Nuremburg trial, that of IG Farben, the fourth largest corporation in the world at the time. Bayer, who now owns Monsanto, was a unit of IG Farben. This (IG Farben) company produced the gas used to slaughter 6 million Jews, gypsies, gays, the disabled, and anyone else the Nazi’s thought impure. By the way, the Nazi’s got some of their ideas about race from the California-based eugenics movement.

Talking Mexico as a horror example I read about a very clever comparison that was done relating to the neurological development of small children by comparing typical pencil drawings from the children living i vallies where they were exposed to high levels of pesticides with the drawings from children of the same age but living higher up on the hillsides with less exposure. The mental retardment of the valley children is so obvious by comparison of these “simple” drawings. I my my mind it is not possible to defend pesticides having seen this.

This scary comparison can be found in the very revealing book The Myths of Safe Pesticides
by André Leu

Industrial pesticides are a real issue of concern. Many of them are toxic to many organisms ( including humans ) not just the target species. And many of them are persistent in the environment.
Examples of these are pesticides from the organochlorine family of chemical compounds such as DDT. DDT is now banned from use in many developed countries. But it is still being produced and used in less developed countries. These pesticides are usually not immediately toxic to humans but cause major long term health issues. They are are very persistent taking generations to break down and having toxic break down compounds as well…

There are also the organophoshate pesticides. These are incredibly toxic..human death can occur in hours..

There is also a newer family of pesticides called ‘Neocotinides’. One of theses is marketed at Confidor in Australia. While supposedly harmless to humans these are the cause of colony collapse in bee populations world wide..Not very clever.. Which is why the EU has banned it’s use outdoors.

Roundup is yet another type of pesticide. It’s supposedly active ingredient is Glyphoshate but the other ingredients are also poisonous.. Ss this is now out of patent and now longer the exclusive intellectual property of Monsanto, it’s made in many countries with differing formulations and maybe added ingredients to increase the pesticide impact…It is now probably the major herbicide used on Earth especially in broad acre crop farming…Here in Oz there is an entire methodolgy of crop farming which avoids ploughing or disking or turning the soil, by using a single tractor pass with a farm implement which sprays the ground with Roundup or similar, to kill weeds and then via second implement sows the seed of the crop. That method is called “No Till” and is touted as a great benefit to the soil as the dead weeds & stubble on the surface prevent soil erosion. However the herbicide spray also kills the micro-organisms in the soil which is not a great idea at all…

There are organic methods of dealing with pests in crops or gardens or orchards.. In fact there are a whole swag of them. They are characterised by not being naturally found in the environment, toxic to humans, not being persistent ( breaking down quickly ) and by targeting the pest species. Thus for example in the past I have used a bacterial formulation from Bayer, in a water based spray, to control pear/cherry slugs on pear & nashi fruit trees…It breaks down quickly, only kills the pear slugs and is perfectly safe to handle. The bacteria was discovered in the soil on an island in the Caribean back in the 1980’s. Pyrethrum used to be used as an organic spray for this but is not as targeted and kills other insect species which are not pests like bees.

The pesticides used by organic farmers & gardeners tend to be more expensive than the industrial chemicals. And that means that the organic produce can be more expensive… But I suggest it’s worth it…

Bill, I had three bee hives in my garden and some years ago they were totally abandoned by the bees and amazingly they had left all their honey behind. I also had a lot of frogs in my ponds but today their are all gone.

Suspicious about what the nearby farmers were up to I approached one of them a week ago asking about this but he just shrugged his shoulders.

Goran, bees going missing from bee hives is the classic sign of neonic use nearby – within a kilometer..The individual bees lose the ability to get home to their hive with nectar & pollen and the hive slows collapses.

Frogs disappearing however is probably due to the spread of a fungal disease ( originally from North East Asia ) in the water of aquariums..It is a world wide problem.Here a number of unique Australian frog species have died out completely…Just for the aquarium pet trade.

Yes I think a lot of farmers have been persuaded that glyphosate damages the soil less than cultivating. I used to use it in the garden using the same logic.

Mostly here apart from the glyphosate, also used for pre-harvest dessication, farmers tend to wait until their neighbours or Crops Advisors warn them of a potential threat rather than doing proactive spraying because of the cost, including the diesel for application. They are also somewhat loath to use neonics when they actually import bees for crop pollination, which is good.

The other side of the coin is crops specially bred for “pest resistance” which contain natural pesticides. Probably eating these is not so good for humans.

Comparatively little pesticide use in animal agriculture, of course, though antibiotics and other drugs may also be problematic.

All what we are up to today relating to Big Agro and Big Pharma activities reminds me of the greek myth of Ikaros who was struck by hubris when he learnt to fly and then went too close to the sun and lost his wings while his cautious father Daidalos didn’t overdo his engineering flying task.

In the end I think the pesticide question is much like other questions. You really can’t battle nature by force. You’ve got to use science to figure out how to work with nature, not try to outsmart it. Can’t be done. Period.

We may be temporarily feeding this big population, but it is the so-called green revolution, i.e., pesticides, herbicides and artificial fertilizer that have been largely responsible for the population explosion. But there is no use staving off an emergency if it is going to just create a bigger one in the future and more people will die and be sick.

I actually think that true, robust health is not possible any more. Perhaps in pockets here and there, but for most people. I mourn for my grandchildren.

But I don’t actually think we need big ag to feed the world. That’s another myth that they put out there. If we had a different approach, we could probably do it. It is amazing how many people want to be small farmers and of course historically they always have. So much food could be grown in gardens and small local farms.

It seems to me that so many have been viewing the LDL/atherosclerosis issue as a one size fits all approach to medicine. High LDL causes atherosclerosis vs. high LDL not causing atherosclerosis. This is similar to stating that too much salt can cause hypertension. In reality, there is just a percentage of people whose blood pressure is affected by salt this way. Over a period of time, high LDL can cause atherosclerosis in some people. In other people, it won’t. In some people high LDL will not show any discernible signs of atherosclerosis. It’s not because they are “protected” by something else; it’s that their individual physiology and metabolism function differently.

Franny G you wrote
“high LDL can cause atherosclerosis in some people. In other people, it won’t. In some people high LDL will not show any discernible signs of atherosclerosis.”
1 : You use the word “CAUSE”
Really mate ? On the basis of what evidence ? I suggest you go back and read a few of Dr Kendrick’s other posts on the actual causes of CVD.

2: The near universal medical response to high LDL-C is the prescription of statins. But if we accept your statement, these will be ‘effective’ in only a proportion of the population.. And statins are toxic for a good proportion of folk…

So your thinking leads to a poison being prescribed for what is a non existent problem !

Fine. But where does this leave “science” if A causes B in some but not in others? I think Dr. K is right to point out that the “theory” behind high LDL being a CVD precursor fails dramatically for some patients, and it is the job of “experts” to tell us who is and isn’t at risk as to lipids.

Wiki: “Occam’s razor (also Ockham’s razor or Ocham’s razor; Latin: lex parsimoniae “law of parsimony”) is the problem-solving principle that, when presented with competing hypothetical answers to a problem, one should select the answer that makes the fewest assumptions. The idea is attributed to William of Ockham (c. 1287–1347), who was an English Franciscan friar, scholastic philosopher, and theologian.”

Occasionally Malcolm you have mentioned the plight of the Indigenous aboriginal people of Australia. And indeed there are some groups within our Aboriginal population who are indeed in need of help. However you tend to be of the view that this ‘help’ should not involve becoming a nanny state. For example the sugar tax in the UK which you disagree with.

My own view is simply ‘do what works’ and today there is this news report which exemplifies the effectiveness of this approach in the Northern Territory. It is not just about the seizure of 185 liters of cask wine.It is also about the dramatic drop in domestic violence incidents etc.

Sad that there are so many contributers of multi-items who seem to have no others interests than needing to have multifarious contributions on this subject. One contributer (nameless.. but apparently ‘big down underr’) seems to have no ther interests and needs to get a life…. !!!???!!

I took a look at your website. I notice that you still list a high saturated fat diet as increasing the risk of heart disease and stroke. “It is estimated to cause about 31% of coronary heart disease and 11% of stroke worldwide.” Huh ?

Recent research shows this assertion to be false. Would you like to explain why you choose to stay with the saturated fat hypothesis ?

Franklin, high cholesterol has benefits.
“The vast majority of the research leads to the same conclusion; low cholesterol leads to higher rates of depression or depressive symptoms. For many with depression suicide is a tragic reality. As low cholesterol is linked to depression, low cholesterol is also a risk factor in suicide attempts.”

Back to the topic of this post : Familial hypercholesteremia.. I have just been reading the Wikipedia entry on FM..And have come away totally confused..It seems, to put it briefly, that the Wikipedia authors on this subject are convinced that persons with FH suffer from CVD at higher rates than the normal population… And there is no mention of Black Swans such as your 72 year old example.
Is it a plot ? What is going on ?

Bill in Oz: Wikipedia is a propaganda platform. It is also a closed system. It is not possible to correct factual errors, as their secret “editors” call the shots. I never use it. There are better sources of information.

Bill in Oz: Correct. It is not all propaganda. Likely that much of it is correct. But nobody is allowed to correct errors except the secret editors, and they have an agenda. Two examples: Philip Roth, the noted author, was not allowed to correct a factual error concerning one of his books. The posting on Dr. Andrew Wakefield is slanderous garbage. Very difficult to win a slander suit. Dr. Wakefield’s against BMJ and its editor, Fiona Godlee, was thrown out of a Texas court on a technicality-the judge bought BMJ’s argument that they don’t do business in the U.S., despite the fact that both online and print versions are available here. I have high standards, and refuse to support any institution which defames people. Virtually everything we’ve been taught about vaccination our whole lives has been propaganda. Discovering this eliminated all trust I once had in our public institutions. By the way, I find history fascinating, too.

AH Notepad: Thanks for the link. I had no idea this was a neo-con operation. These are the folks who have essentially destroyed the Middle East, and they include the fresh set of alligators Trump has brought right into the swamp (such as John Bolton, George “Dubya” Bush’s right hand man, and who recently scared the bejeezus out of Kim Jong Un on the eve of an historic summit by implying he would get the Ghadaffi treatment). Bill in Oz, I don’t know how much you know of the politics involved here, but it is ugly. I favor no political party or persuasion, just right over wrong. It is simply wrong for snipers to fire live ammunition at unarmed demonstrators in the open-air concentration camp called Gaza, killing many and injuring thousands. Are the neo-cons in high places in the U.K. government now?

The neocons are everywhere. They are after total control. John Bolton, bad as he is, is only one of their minions. They started as the Illuminati. The Rothchilds might ring a bell or two. They control Europe, middle east, soon……………..everywhere. See Blackstone Intelligence on youtube.

Bill in Oz: When I do a DuckDuckGo search I get lots of results. I think the Britannica has an online presence, although we have the last print version. I just use discernment. There are still plenty of honorable people in this world. Those who are attacked for their views are often more reliable than the attackers. The media has always been to some extent unreliable, since all editors, like the rest of us, have biases. Today, multi-national corporations have a high level of control over most governments and the media, as well. None of them can be trusted (government and media).

Dr Kendrick great writeup. From BMJ – Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis …. http://bmjopen.bmj.com/content/6/6/e010401.full

Isn’t there something fundamentally wrong with our education systems that leads to the reluctance of people to think for themselves? Don’t we still put too much emphasis on remembering and regurgitating facts and passing exams? Why are people so scared to inquire into areas they haven’t been examined in? Why are they frightened to read about medicine or the universe except in the tabloid papers? And why are others criticised, sidestepped or ridiculed for daring to inform themselves properly? Years ago people were encouraged not to live “beyond their station”. We are still being held back, but in our thinking. Plenty who read this blog think outside the box – thank goodness.

TS: I think that there is indeed something fundamentally wrong with our educational system, that is our public educational system, and that this has been true from its beginnings in the late 19th Century. If you want a more positive view of how people for a very long time have educated themselves through the act of reading, I recommend Jonathan Rose’s “Reader’s Liberation,” published early this year by Oxford University Press. From the Preface: It is a “. . .broad narrative history of reading. . . . And this story has a central theme: that reading can be and has been the most fundamental expression of human freedom, even in repressive societies.”

I was interested to read you have been taking niacin for about a year. I’m mulling over adding niacin to my supplementation and was wondering if you could tell me what you take and how you got on with it initially because:

1. there seem to be recommendations for and against slow release niacin supplements and also
2. any problems with the niacin flush?

Mainly, I’m dithering because I can’t make out whether it’s good for plaqued up arteries in general or the lp(a) element of plaqued up arteries. I think there is a comment or a link to a comment in this current blog stating in some trial a 30% reduction in lp(a) levels.

You mentioned testing…or lack of. Were you talking about its effect on your lp(a) levels?

Charles, I have been taking 1000mg tablet each day for the past year…because I read that it is beneficial for folks with CVD issues. Rogue Health had a major article onit around March last year..I don’t take the slow release version Just straight B3 and I have had no niacin flush issues at all.

B3 is a very beneficial supplement..I think…But there is no money in it for pharmaceutical companies as it is not on a patent…

I was hoping after 12 months to see if there was any CAC reduction as my level was high in late 2016…But I have not been able to get a referral to get it tested again…Ummmm !

I have many patients who have normal standard values (cholesterol) but have developed advanced coronary heart disease at an early age despite following a perfect lifestyle (not smoking, regular aerobic exercise, healthy diet.) The skeptical cardiologist tests such patients for Lp(a) Our best drugs, the statins, for reducing risk of heart attack and stroke also don’t lower Lp(a) levels. It is the strongest single inherited (monogenetic) risk factor for the early development of coronary artery disease, heart attacks and strokes. https://theskepticalcardiologist.com/

Sickle cell disease increases the risk of premature CVD by up to 50,000%. Thus, whilst I agree it has an important role, I would question raised Lp(a) as being the strongest inherited risk factor for the early developed of CVD.

Machine learning is the process of taking lots of data about a subject, splitting it into around 75% and 25% and then training the computer on the 75% where it knows the result we want to predict eg did someone get heart disease, and then asking it to make predictions on the unseen 25%. We can then see how good it was at predicting on the fresh 25% but more importantly we can also get the computer model to tell us which variables were deemed the most important out of the variables it was using when ‘learning’ how to predict. This form of machine learning has been used to defeat world chess champions and makes predictions on a huge array of other automated predictions we know take for granted. OK so why the ML lesson ?, well it has been applied to predicting heart disease. Using thousands of patients who initially has no signs and then logging those that developed heart disease 10 years later, the machine learning alogorithm was let loose on the data. If performed better than conventional prediction method thrown at us by our doctors but of real interest was the top 10 risk factors. They used four different types of ML program and in none of them did LDL cholesterol appear in the top 10 risk factors. HDL appeared in two of them and Triglycerides in one of them but LDL appeared in NONE of them.
You can read the paper herehttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0174944

Indeed! What is required to shake someone’s conviction when they are convinced! I’m not 77, but my total cholesterol is 278 (tested two weeks ago) and my CAC score is 0.0 (same day as blood test). How many times and in how many ways do we have to say it: cholesterol does not cause heart disease.

FTL: He backed his concerns with medical records, including a Royal Free discharge summary.5 Although the family lived 5000 miles from the hospital, in February 1997 the boy (then aged 5) had been flown to London and admitted for Wakefield’s project, the undisclosed goal of which was to help sue the vaccine’s manufacturers.6
Wakefield’s “syndrome”

Unknown to Mr 11, Wakefield was working on a lawsuit,7 for which he sought a bowel-brain “syndrome” as its centrepiece. Claiming an undisclosed £150 (€180, $230) an hour through a Norfolk solicitor named Richard Barr, he had been confidentially 8 put on the payroll two years before the paper was published, eventually grossing him £435 643, plus expenses.9

KidPsych, I don’t understand what the point you were trying to make, but since you quoted from the reporter, brian deer, (capitals not deserved) who was employed by The Times, whhose owner, James Murdoch was on the board of directors of GlaxoSmithKline, manufacturers of the MMR vaccine, I think we should be told.

KidPsych: Logical fallacy #4: Ad Hominem Argument. In more colorful language,”shoot the messenger, ignore the message.” Is this what you are advocating? I suggest you actually read the science amassed by the World Mercury Project.

I’m not aware – nor have I had any reason to look – of the details of Wakefield’s behaviour that would render his suspicions as being ‘unsafe’. Far more relevant is the proven dishonest behaviour of Merck and their MMR vaccine ‘efficacy’ claims, – seemingly ignored by the US FDA and CDC.
The continual interchange of executives and ‘scientists’ between these agencies and Pharmaceutical companies is equally abhorrent.
However, I would not suggest KidPsych takes a shot at the FDA or CDC, as the US military generously donates surplus weapons etc to any and all Law Enforcement agencies merely for the asking., thus giving “vaccine shot” a whole new meaning !

Further to Notepad’s comment on your ad hominem ‘argument’ style – is that journalist from the same newspaper group involved in that ‘mobile phone hacking’ scandal ?
I would equate their deceit on a par with a ‘Health-focused Church’ that infiltrates Dietiticians and other medical associations with their ‘Revelation-derived’ dietary dogma of plant-based “salvation” !

If I may sneak a Royal Wedding post under the radar, Saturday was my 70th birthday which we celebrated by watching Harry and Meghan get married, followed by the FA Cup final to get some exercise. So when I read this at your link I paid attention:

Between 1995 and 2010, the proportion of adults getting five or more drugs doubled to 20% . Le Fanu describes how this ‘prescribing cascade’ can happen. How in a matter of months a fit 70-year-old man put on a statin simply on the basis of his age, could be on six drugs.

Following the statin, he begins to suffer muscle pains. So an anti-inflammatory is prescribed to help. One effect of these drugs is to raise blood pressure, which shows up at his next doctor’s appointment. This leads to a blood pressure pill (diuretic). A few months later a very painful case of gout develops which is a known effect of diuretics. Weeks later raised blood sugar shows up (another side effect of diuretics) so he is put on the diabetes drug metformin which leads to a diarrhoea and another drug prescribed to help with that.

It is worrying. I’m not on any medication. My doctor put me on statins years ago. I never took them because I researched them on the internet and found this site, and so far (touch wood) so good. But when should you ignore your doctor and when should you follow his advice? A little medical knowledge may be a fatal thing.

My policy is to keep as healthy as I know how to be, stay away from the doctor if there’s nothing wrong with me, not get flu shots, and not get checkups if I don’t have any symptoms. Although I wonder if the odd colonoscopy and prostate exam might not be a good thing.

I fully agree with your desire to steer clear of the medical mafioso, but sometimes fate intervenes. In my 71st year I had a MI, which resulted in being put on 4 powerful meds for an indefinite time. When I reported nasty side effects to my GP, he responded by trying to start a drug cascade. Luckily, I managed to convince my cardiologist that I wasn’t going down that route, and he kindly left me on one single med for the time being. We had a robust discussion about statins, which he would really wish me to take, but I do believe he realized he was beating a dead horse on that one!

Bill,
I think you are too cynical. I respect my GP’s skill at diagnosis, which is far better than my own. He is quick to write prescriptions, but I am just as quick to ignore them.

He once prescribed me antibiotics for a case of flu. I queried this, saying I had heard that antibiotics were useless against a virus. He said I was correct, but patients expected antibiotics so he prescribed them. Basically, he was using antibiotics as a placebo. Maybe other doctors use medication in the same way.

The thing is, for every person who thinks cholesterol is good and statins are bad, there are probably ten who think the reverse. And if a doctor won’t prescribe them statins, they’ll go to another doctor. Faith in statins (and antibiotics and antidepressants) is so pervasive, it’s difficult for a doctor to resist the demand for them.

David I do not agree with polypharmacy either..I think it is dangerous and rather stupid. It only serves to maximise pharmaceutical company sales..

By this study relies completely for it’s conclusions on ‘Creating a synthetic UK’ so as to be able compare what actually happened under this program with what would have happened if it had not been done…

Ummmmm ? And that means total & complete mystification for 99.9% of us….

Sorry, not good enough David….Let’s stick to the real world. It provides far better evidence.

I think that seeking to find parallel real live countries, provinces, states or regions which did not take part in or have a QoF regime would allow a real comparison..
There is no QoF type program in Australia. Doctors here don’t precribe such drugs because they get government inducement to do so. ( Unfortunately they do it because they are true believers !)

And there other countries which could be useful parallels. Eg. : New Zealand & Canada ( with the probable exception of French speaking Quebec ).
And what about the Republic of Ireland ? My understanding is that in Ireland people needing a doctor’s consultation pay for the consult though they may get a refund from private health insurance. So no doctor gets paid for prescribing stuff like statins, BP med. etc…
And was the QoF program implemented in Gibraltar or the Channel Islands ? ( I am not sure if they are part of the NHIS in the UK ) ..They are small in terms of population but would still offer a real comparison. Not a synthetic one.

Malcolm, how about comparing areas served by QOF – High Performing doctors, with similar folk whose Medicos are “Rx impaired” GPs.
– prescription cost per patient. Vs overall health/ all cause mortality ?
Or NNT. renamed as. $ NT
Would that work ?

Sorry mate, no they did not. The link states
1:” Researchers from Michigan School of Public Health in the USA and from Manchester and York Universities in the UK gathered data on mortality and chronic disease in similar western countries without a medical pay-for-performance system.”

2 ” Then they used that to create a ‘so-called synthetic UK as a weighted combination of comparison countries.’ The synthetic UK – the results that could be expected without QOF – were then compared with the result in the real UK ”

I have no idea if they ‘doctored the data’ or not. In fact despite the fact that I did 2 years of statistics at uni decades ago, I have not the advanced statistical skills or interest to know if they doctored the data. .

But the comparison was between a ‘synthetic UK’ which does exists only in their study, with the real one where you live.

I think the point is that had that study demonstrated that QOF gave us huge benefits, it would have been splashed over all the newspapers. As it is, it was hidden. It is surely worth every doctor realising just how evidence is filtered to accentuate the positive before they see it!

Also, if it is too flawed to be able to tell us anything, why was the research ever performed or published! Part of the scandal with bad science is research that can be exploited if it comes out the ‘right’ way, and safely buried if it comes out the ‘wrong way.

This might act as a dose of common sense when doctors contemplate the latest idea to collect vast amounts of medical data to use machine learning to discover even better ways to treat us!

I looked at these as the result of a recent experience. A few days ago we went up a mountainside in a cable car and walked back down the steep path. Half way down both my knees screamed “no more”. My husband is not keen on giving piggybacks so I was stuck. Instinctively, or because there was nothing else to be done, I began walking backwards. No pain at all! What interested me most is that the back of my knees are still feeling the effects of the stretching (which my GP recommends anyway for cramp). It was clear that I was using muscle that I don’t normally exercise.

I have toyed with the idea of developing a walking back downwards machine for use in Gyms for a while (just have no idea how to go about it). Almost all exercise machines are ‘go forward’ or ‘go up’. There is nothing for going back down again. I do quite a lot of hill walking, but it is the going down that can be the killer, especially if you have not done it for a while. So, not sure about going backwards, but we absolutely do need to balance up our exercise a bit more.

I tried going down the up escalator at the shopping centre. Facing uphill, I found I had to take awkwardly large steps backwards because of the fixed run and rise of the escalator treads. Facing downhill was easier, almost like running. But the other people on the escalator were quite a nuisance, so I couldn’t keep it up long enough to get some decent exercise.

Any commercial apparatus would need to be infinitely adjustable to fit each person’s individual stride length.

TS: Very interesting, indeed! My only marathon was a downhill run (average 2% grade). At mile 21 my right-side ilio-tibial band screamed at me to stop. The last 5 miles were a run-walk. On my weekly hikes the going up, while slower, is easier than the coming down (mostly 5-10% grade), so I have to build up my downhill strength beginning in the Spring. And I remember from my alpine skiing days training for it by lots of downhill walking in the fall. Backwards walking I haven’t attempted since childhood, and it would concern me without a companion. You will be up on your toes, which will indeed stretch the calves and hamstrings.

Mr Chris: Heat really helps with injured muscles. Probably works with tendons, too. As far as rehab, go easy; increase slowly and allow for recovery. Inflammation from muscle building lasts a full four days. I find a 48 hour recovery period sufficient for my workouts, but not all the time; sometimes it takes four days. I had my most strenuous hike of the season (so far) today. Six mile (~10 Km) roundtrip, with an elevation rise of 2,200′ (670 m). 14% grade. Going up was easy, and coming down not bad, although I kept thinking about TS’ experience, and worrying a bit on the steep parts. I do have really strong legs from 23 years of running, but I did stop a few times on the steep parts because my quadriceps would get fatigued. Didn’t want them to fail me altogether, as I hike solo. I usually see a few people, sometimes a lot, and thoroughly enjoy meeting new fellow hikers, but today, not a soul, just squirrels, lizards, and lady bugs. Took 5 hours.

“Something for people trying to improve their muscles and joints? (E.g. After statins?)”

This raises an interesting (and very important) question. Some people report statin damage that doesn’t go away when they stop the drug, and I wonder if exercise facilitated by pain killers is the answer. I just gradually phased out the pain killers as I recovered. This is what worked for me, but I am just one data point!

Many years ago (long before I was offered statins) I got into ice skating. I have a polio leg, and I need to use an ankle brace to make this possible. My feeling is that this is also an excellent form of exercise – particularly for the back muscles. It also really tunes up the sense of balance!

I’ve just figured out how to make a comment rather than a reply. An old dog can learn a new trick or two. I’ve been looking at Kauffman’s charts of statin trials. I recall Dr. Kendrick writing that the only non-industry-funded trial was negative, and it seems to me he said it was ALLHAT, which was pravastatin. In the chart there is virtually no difference for non-fatal heart attack between treatment and placebo groups (AR -0.1). If we factor in that trials use a select group who tolerate them well, but the drugs is dispensed to everyone foolish or uninformed enough to actually take them, this is an alarming finding. The results for all-cause mortality are not much better (AR -0.6). The hands-down worst of the bunch, though, is lovaststin. In both trials (EXCEL and AFCAPS), the treatment group succumbed quicker (+0.3 for EXCEL and +0.09 for AFCAPS). Yikes!

Way back when I was actually seeing a cardiologist, I asked about pravastatin because it presents the least risk of developing diabetes. He said “Oh, that’s not effective. We don’t prescribe that at all.”

Frederica Huxley: Going down forward will strengthen those muscles nicely. Going down backwards would be fine and dandy, but TS only did it that way because she couldn’t go forward. A charming solution to a scary problem.

Tomorrow, May 22 is The International Day for Biological Diversity (IDB) and me and my wife will participate. I guess we are not only metabolically adopted to diversity but also to use all of our muscles in a non-monotonous way. Exercise is for sure a biological activity and could thus be celebrated tomorrow as well.

The garden work is very diverse and where going backwards is certainly an important part and probably also very good for my CVD.

At the University of Gothenburg “The International Day for Biological Diversity” was celebrated in various ways, among which there was a discussion among a few researchers involved int their “Center for Global Studies of Biological Diversity” and us lay participants of the public.

The sad thing is that this “discussion” reflected the same type of “holy” consensus stupidity among these biologists as would most probably bee seen among “official medicine men” in a consensus debate about cholesterol.

The reality of the devastation of our fertile soils world wide was evidently a too big an elephant to be brought into the debate – the consensus agenda was set from the very outset “as usual” and, of course, if you close your eyes hard enough you may make reality disappear perhaps with the help of a complacent “postmodernist” philosopher as was present yesterday.

JD Patten: Excellent idea, with the Empire State Building as the PhD thesis. During our marathon training, one of our activities was running up and down the university football stadium steps. Some made it all the way around, every step, but I bailed at the halfway point. No heroics from this kid. I was 55 then.

Off topic. B-S**t alert.In todays Times. British Journal of General Practice says that people would be more inclined to stick with the statins if their doctors were more inclined to talk soothingly and sell it as a way to take control. Of course BHF says “great idea”.
They don’t impress me.

Dear Bill in Oz
I have no trouble from my GP – I am very lucky. He is kind, and caring, and (over) cuddly – to the extent that if he were ever to say anything about the benefits of losing weight, I would stare very hard and pointedly at his middle section! He has also said, in plain English, that he thinks statins are pretty evil drugs. I wish I could get a GP like him for everyone who is trying thoughtfully, to make the best of a bad situation, in regard to health. The other thing I wish is that it was not such a pain trying to get an appointment.

Gary thanks for the source.. A couple of comments
1; I am more interested in this vaccine’s impact on Cardio vascular health than how it performs as a reducer of pneumonia infections..

2 I looked through Mooney’s paper. And he makes an interesting point.However it is clear that he is comparing the incidence of pneumonia reports in the Winter of 2003-4 with the reported incidence in the previous 4 years..

This 23 valent pneumococcal vaccine has been around for quite a while..a decade or more. So we are looking at population with a large number of individuals in who have already been vaccinated in previous years – especially in those susceptible such as the younger age groups & elderly.

My point is that this is not a naive population which has not been innoculated with pneumonia vaccines before……Which has then in Winter 2003-4 been vaccinated…

There is thus no true comparison of effectiveness or lack of it…

There may be reasons for not having this vaccination.But this study is not good evidence to support such a reason.

Bill in Oz: To me this study is nothing more than an addition to the body of evidence. I just realized, looking at the U.S. Vaccine Excipient and Media Summary, that PPSV-23 (Pneumovaz) is licensed in the U.S. The only excipient listed is phenol, whereas PCV13 contains, among other things, aluminum phosphate. I just listened to a Del Bigtree interview with both Professor Chris Exley and Dr. Yehuda Shoenfeld, who were part of the Auto-immunity Summit in Lisbon. We should all be concerned about ingested Al, and especially about injected Al salts, which the majority of childhood vaccines contain.

Thanks Gary for that tit bit of good information
For “PPSV-23 (Pneumovaz) the only excipient listed is phenol, whereas PCV13 contains, among other things, aluminum phosphate.”

Now that is useful to know as I agree that aluminium salt in vaccines should be avoided…

But I still think that when assessing a study like the one you found, the context needs to be taken into account.
When vaccines were first thought of ( say Dr Jenner with his for Smallpox in the 1789-90’s) there was a population which was extremely vulnerable to the disease..And the disease had a high mortality rate.. So the vaccine, even though primitive by our standards, was successful.

Now we have national populations where almost all have been vaccinated for a range of infectious diseases, often as young children..And so the additional benefit of any new vaccine becomes lowered…

While simultaneously the infectious diseases themselves often evolve and the old vaccines may become ineffective.

This is not a simple subject…

But avoiding toxins such as aluminium salts in any vaccines is a first priority..

Bill in Oz, you will find a comprehensive history of smallpox vaccination in “Dissolving Illusions” by Suzanne Humphries and Roman Bystrianyk. It will be interesting for you that the vaccinations were stopped in Leicester after a revolt, and the disease rate dropped, whereas in surrounding towns it continued unabated. Something that will tell you about Jenner may shock some, and surprise others https://globalfreedommovement.org/5-historical-vaccine-scandals-suppressed/
To say vaccines were “successful”, you would have to define what is meant by “success”. For reducing disease the claim is contentious.

AH Notepad: Thanks for the link. I’ve been puzzling over the thought that some can recognize the quackery in statins, but not question vaccination. I attribute it mainly to lack of knowledge. So many fairy tales we have been repeatedly taught throughout our lives they become unquestioned truth.

Bill in Oz: Sorry about the mis-spelling of Pneumovax. The Edward Jenner story is largely a fairy tale. He was actually a late-comer to variolation. It had been attempted in England twice before, in the late 1720’s, and in the 1740’s. Both times it died out after a short period. Jenner, though, had political connections. His “clinical trial” was the stable boy, who survived the ordeal with no apparent adverse effects. But the practice was so dangerous and ineffective that by 1885 the good people of Leicester rebelled, held a mass demonstration, stopped vaccinating, and essentially made the problem go away. How did they do it? Sanitation, isolation of contacts, and home quarantine of the cases. Why did the British Parliament overturn the mandate in 1907 (if it was so effective)? Details in “Dissolving Illusions.” Why has this practice persisted, and rapidly expanded in recent decades? It has always been lucrative, and liability for injury doesn’t exist in the U.S., and is hardly enforced in the U.K. As far as I am concerned, vaccination is a horrid example of medicine gone wrong. The fact that they target infants and children, who may be too young to understand or describe their injury, makes the industry, in my opinion, diabolically evil.

“Our study supports the notion that people who are unable to do load-bearing exercises — such as patients who are bed-ridden, or even astronauts on extended travel — not only lose muscle mass, but their body chemistry is altered at the cellular level and even their nervous system is adversely impacted,” says Dr. Raffaella Adami from the Università degli Studi di Milano, Italy.

The study involved restricting mice from using their hind legs, but not their front legs, over a period of 28 days. The mice continued to eat and groom normally and did not exhibit stress. At the end of the trial, the researchers examined an area of the brain called the sub-ventricular zone, which in many mammals has the role of maintaining nerve cell health. It is also the area where neural stem cells produce new neurons.

Limiting physical activity decreased the number of neural stem cells by 70 percent compared to a control group of mice, which were allowed to roam. Furthermore, both neurons and oligodendrocytes — specialized cells that support and insulate nerve cells — didn’t fully mature when exercise was severely reduced.

The research shows that using the legs, particularly in weight-bearing exercise, sends signals to the brain that are vital for the production of healthy neural cells, essential for the brain and nervous system. Cutting back on exercise makes it difficult for the body to produce new nerve cells — some of the very building blocks that allow us to handle stress and adapt to challenge in our lives.

“It is no accident that we are meant to be active: to walk, run, crouch to sit, and use our leg muscles to lift things,” says Adami. “Neurological health is not a one-way street with the brain telling the muscles ‘lift,’ ‘walk,’ and so on.”

The researchers gained more insight by analyzing individual cells. They found that restricting exercise lowers the amount of oxygen in the body, which creates an anaerobic environment and alters metabolism. Reducing exercise also seems to impact two genes, one of which, CDK5Rap1, is very important for the health of mitochondria — the cellular powerhouse that releases energy the body can then use. This represents another feedback loop.

These results shed light on several important health issues, ranging from concerns about cardio-vascular impacts as a result of sedentary lifestyles to insight into devastating diseases, such as spinal muscular atrophy (SMA), multiple sclerosis, and motor neuron disease, among others.

“I have been interested in neurological diseases since 2004,” says co-author Dr. Daniele Bottai, also from the Università degli Studi di Milano. “The question I asked myself was: is the outcome of these diseases due exclusively to the lesions that form on the spinal cord in the case of spinal cord injury and genetic mutation in the case of SMA, or is the lower capacity for movement the critical factor that exacerbates the disease?”

This research demonstrates the critical role of movement and has a range of potential implications. For example, missions to send astronauts into space for months or even years should keep in mind that gravity and load-bearing exercise play an important role in maintaining human health, say the researchers.

“One could say our health is grounded on Earth in ways we are just beginning to understand,” concludes Bottai.

Story Source:

Materials provided by Frontiers. Note: Content may be edited for style and length.

Gary
Backward walking is certainly doing me good , no night cramps so that must be to do do with slackening the bottom of the calf muscle. My wife finds it makes her feel dizzy, and I find it requires quite a mental effort.
Now a bit more on topic, when I was on speaking terms with my lipidist he told me a side effect of some statins, was to induce tendinopapthy. I puzzled a bit over the mechanism for that and came up with a theory that the muscle weakening put more of a strain on the tendons? What do you think?
What I like about this blog is what I learn from it, to cite another example, Göran consumes a lot of vitamin E, and I sometimes suffer from palpitations, a racing heart. I decided to give 800 iu of vitamin E a go, since when no palpitations.

Mr Chris: That sounds like a reasonable supposition. It could be, too, that whatever mechanism weakens the muscles weakens the tendons as well. Good for you that the backward walking and vitamin E are helping. The body is good at healing itself if we give it what it needs and avoid what is damaging. It pleases me to continue to learn, after paying close attention all these years, what is the proper type and amount of physical activity to achieve optimal health. I really thought about TS’ experience on my hike this week. Going up on steep ground, I often make 30 second pauses to let my heart rate come down a bit. This time I did the same a few times on the steepest stretches, to let my quadriceps recover. Didn’t take long. The sweet spot. Not too much, not too little. Goldilocks.

Mr Chris
Good!
I’ve been alternating forwards and backwards – about 20 steps forwards followed by around 20 backwards (when feasible!) and although it’s early days, I’m encouraged too. Get a few smiles (or giggles, but never mind).

Most interesting. Read it once, will need to read again. But it appears to confirm two things. 1: high levels of insulin damage the endothelium, leading to atherosclerosis. 2: The primary damaging effect appears to be on reducing NO synthesis.

If true, and these findings are supported by a lot of other research. We absolutely must work hard to reduce insulin levels in those with diabetes (HFLC)/exercise/sunshine/vitamin D. And we absolutely must move away, as much as possible, from using more and more insulin in type II diabetics.

Of course the current mainstream medical guidelines recommend the absolute opposite

I am a great lover of “thick” books written by serious authors not least of medicine and I am now taken by a book “The End of Alzheimers – The First Program to Prevent and Reverse the Cognitive Decline of Dementia.” This is for sure a controversial title but the author Dr. Dale Bredesen is a professor neurology of the University of California, Los Angeles and has been in the research of this field for thirty years and apparently knows what he is talking about.

Dr. Bredesen seems in my eyes to have a clearly scientific approach to the subject and has arrived at a holistic view (similar to my own) where he find at least 36 factors involved in Altzheimer’s which must be adressed simultaneously.

Among these factors excess insulin is an important culprit and an interesting point Dr. Bredesen is making is that the breaking down of the insulin is carried out by the Insulin Degrading Enzyme, IDE, which is also the enzyme that breaks down the beta-amyloide involved in Altzheimer’s and can’t do this when insulin levels are high.

What he arrives at is basically a strict LCHF regimen and a lot of vitamin supplements as the remedy. You may understand why I am taken by this book since it coincides with how we treat my CVD and the T2D of my wife.

I also find this panacea approach strongly endorsed by this Sunday morning newsletter from Dr. Mercola in which he is taking a strong position on the importance of vitamin and other supplements for older guys like myself – all about proper nutrition.

Dr. Mercola is making a good living on his supplement business but this does not necessarily invalidate what he is saying in my eyes. Usually I find his standpoints, although often controversial, well supported by science as I understand it.

I am sure if I were to take the recommended dose of each of that very abbreviated list, I’d suffer from extreme ‘polysupplementism’ and not feel too well at all – and yet the evidence that each is necessary doesn’t seem to allow for our needs to be satisfied by a subset! For example, suppose I were short of selenium, there wouldn’t be any way to correct that but to consume something with selenium in it (in suitably trace quantities – otherwise it is a poison!).

Getting the balance of nutrition has certainly been made difficult by our dreadful practices.
Although we’ve been chucking and seeping our waste products and chemicals into the sea, the sea is still probably a better bet than land. After all, we did all evolve from it and the area of sea is greater than that of our continents.

The Japanese as a race do well and each one is purported to consume on average over a kilo of seafood a week. Then there is all the seaweed they eat – apparently around 100,000 tons a year between them.
So wild caught shrimps/prawns are top of my list.

But this is getting onto diet again so better not forget how much the Japanese love karaoke!

Soil degradation and chemical residues have savaged the micronutrient balance in our foods. – and utilising deficient soils doesn’t help. For example, my State is mostly lacks selenium. Zero…
Add to that our pollution and ‘strain’ burden which would exacerbate.these shortages and turn a minor depletion into serious dysfunction.

Nobody seems to have addressed my point, which is that there are so many supplements available now – with cogent arguments that they are necessary for health – that taking all of them would almost certainly make you ill – I am guessing, I certainly haven’t tried the experiment!

Since they are all claimed to be essential for health, how does anyone select a subset to consume on a rational basis?

David,
1 : I do take quite a few supplements & minerals. But I am not sick; I am fit, I dance tango, I am healthy, with full head of hair; I think I am also mentally still at my top – though you may beg to disagree. I will be 71 this year…
2 : All the supplements I take are available in nature as hormones naturally produced in the body, from food, herbs or the soil. None of them are pharmaceutical industry concocted chemicals… This has the advantage that they have all been ‘consumed’ by humans for a long time and the dangers worked out.
3 : Thus I suggest your comparison of supplements with pharmaceuticals is misplaced…
Though I note that Willow Bark a beneficial traditional herbal medicine has been used as a template to make aspirin by the pharmaceutical industry and which does have dangerous side effects which I know about personally.
4 : Despite all this, I also suggest your hypothesis that “Poly-supplements” is dangerous is something that you should investigate for your own benefit by trying out the various supplements mentioned here and then trying out various combinations.
But please keep us all abreast of the results of your investigations !

Supplements are like any other manufacturing industry. They need to make a profit, and where social and other factors do the selling for them, the normal ‘Cost + Profit-margins = Retail price’, gets the additional ‘Multiply by What the Market will Bear’. keeps the price up.
– Informed consumers and competition pulls it down.
Simple.
A high % of my supplements come via the USA. Cheaper than local discounters in Oz.

David, cost is an issue.. In the past I have chosen to pay what was needed.. But recently someone here suggested looking at https://www.createyourownsupplement.com.au/
I did so. The cost is about 20-30% of the tablets & capsules sold by companies like Iherb and Vitacost..

Pauling was introduced to Vitamin C when in his 60’s and lived till 90 or so.
Good excuse to add the Pauling – Rath protocol to your anti- aging recipe 😉
That it works through supporting the endothelium benefits us particularly.

Yes AH, she’s brilliant. She also supports synthetic Vit. C as being as useful and safe.
– I feel the important observation is… Goats have a very high natural production of Vit. C, 10 to 12 GRAMS per day, and many times more during stress.
Goats are rarely affected by illness, and never suffer fatal CVD.

Janet, I just had to check if I have any goat chromosomes in order to benefit from Vitamin C supplementation. Human/goat genome comparison has not been completed. Maybe I have more in common with the rattus family. I do believe in evolution.

Janet I tend to take lots of Vitamin C ( 10-12 grams a day for a couple of days ) whenever I feel a bit ‘off… ‘ Lysine is a dailt supplement..While proline I have not yet found anywhere locally to try out..But still looking.

When I’m feeling diligent I’ll follow up on his references, and so far he’s come up fine. Yes, his expression can be somewhat ‘tabloid’, however he is effective in communicating the distilled message!
His selling of better & sharper ‘steak knives’ is simply the American imperative in turning any and every opportunity into a bu$iness plan.
– they just can’t help themselves. 🙂

If he doesn’t bring up aluminum then I am a bit confused. I recently came across an article with a title something like – No aluminum, no Alzheimer’s. It said that certain people cannot detoxify aluminum easily and it builds up. Others may have a similar exposure but are able to eliminate it. Nonetheless, those who don’t eliminate it well would not need to get Alzheimer’s if they didn’t get the toxic exposure.

Two things grabbed my attention because they coincided with some general browsing elsewhere:

1. He mentioned vit C and I recall that you mix up a batch and sip away at it during the day. While browsing the Vitamin C Foundation website (Forum section), there was a comment from the Foundation about why they don’t offer topical vit C products, one reason being “vitamin C doesn’t last long in solution (degrades by 50% in 4 hours)” and

2. Grow your own for nutrient dense produce. Commenters here have posted plenty of information about the decline in nutrient levels in food over the decades, or compared to what our ancestors were eating. I found this on Dr Matthias Rath’s revamped website while browsing for info on niacin:

I guess everyone agrees on that you need many different kinds of micro-nuitrients but in our western food environment we tend to become short of many of them for our physiology to work optimally. But what is enough of each one of them?

For myself I have taken a cautious attitude and probably taking much more than I need through supplements. I am now on 15 g/day of vitamin C and sipping that throughout the day as you mention. Am I overdoing that? I don’t know.

When it comes to vitamin E (mentioned as important by dr. Bresden) it must be of the natural mix and at 2400 IU/day my angina doesn’t seem to be a big problem today.

David,

No-one has died of “oversupplementation” as far as I know although Big Pharma is constantly warning about this while innumerable succumb to their own prescribed drugs.

The gene called Titin—-a certain faulty version of the gene plus alcohol consumption leads to an increase in dilated cardiomyopathy—–

The researchers investigated faulty versions of a gene called titin which are carried by one in 100 people or 600,000 people in the UK.

Titin is crucial for maintaining the elasticity of the heart muscle, and faulty versions are linked to a type of heart failure called dilated cardiomyopathy.

Now new research suggests the faulty gene may interact with alcohol to accelerate heart failure in some patients with the gene, even if they only drink moderate amounts of alcohol.

The research was carried out by scientists from Imperial College London, Royal Brompton Hospital, and MRC London Institute of Medical Sciences, and published this week in the latest edition of the Journal of the American College of Cardiology.

The study was supported by the Department of Health and Social Care and the Wellcome Trust through the Health Innovation Challenge Fund.

In the first part of the study, the team analysed 141 patients with a type of heart failure called alcoholic cardiomyopathy (ACM). This condition is triggered by drinking more than 70 units a week (roughly seven bottles of wine) for five years or more. In severe cases the condition can be fatal, or leave patients requiring a heart transplant.

The team found that the faulty titin gene may also play a role in the condition. In the study 13.5 per cent of patients were found to carry the mutation — much higher than the proportion of people who carry them in the general population.

These results suggest this condition is not simply the result of alcohol poisoning, but arises from a genetic predisposition — and that other family members may be at risk too, explained Dr James Ware, study author from the National Heart and Lung Institute at Imperial.

“Our research strongly suggests alcohol and genetics are interacting — and genetic predisposition and alcohol consumption can act together to lead to heart failure. At the moment this condition is assumed to be simply due to too much alcohol. But this research suggests these patients should also be checked for a genetic cause — by asking about a family history and considering testing for a faulty titin gene, as well as other genes linked to heart failure,” he said.

He added that relatives of patients with ACM should receive assessment and heart scans — and in some cases have genetic tests — to see if they unknowingly carry the faulty gene.

In a second part of the study, the researchers investigated whether alcohol may play a role in another type of heart failure called dilated cardiomyopathy (DCM). This condition causes the heart muscle to become stretched and thin, and has a number of causes including viral infections and certain medications. The condition can also be genetic, and around 12 per cent of cases of DCM are thought to be linked to a faulty titin gene.

In the study the team asked 716 patients with dilated cardiomyopathy how much alcohol they consumed.

None of the patients consumed the high-levels of alcohol needed to cause ACM. But the team found that in patients whose DCM was caused by the faulty titin gene, even moderately increased alcohol intake (defined as drinking above the weekly recommended limit of 14 units), affected the heart’s pumping power.

More research is now needed to investigate how alcohol may affect people who carry the faulty titin gene, but do not have heart problems, added Dr Paul Barton, study co-author from the National Heart and Lung Institute at Imperial:

“Alcohol and the heart have a complicated relationship. While moderate levels may have benefits for heart health, too much can cause serious cardiac problems. This research suggests that in people with titin-related heart failure, alcohol may worsen the condition.

“An important wider question is also raised by the study: do mutations in titin predispose people to heart failure when exposed to other things that stress the heart, such as cancer drugs or certain viral infections? This is something we are actively seeking to address.”

Story Source:

Materials provided by Imperial College London. Original written by Kate Wighton. Note: Content may be edited for style and length.

Errett that is an interesting study.. I read this bit with especially as important :’
The team found that the faulty titin gene may also play a role in the condition. In the study 13.5 per cent of patients were found to carry the mutation — much higher than the proportion of people who carry them in the general population.”

However this leaves the obvious question unanswered : “what percentage of the general population have the faulty gene ?’ I don’t see any answer to it.. And it may vary across the globe in populations with different genetic backgrounds…

13.5% of dilated cardiomyopathy patients with alcohol abuse do carry the gene, and 86.5% of patients do not carry the gene. That is not a remarkably strong association anyhow— but—

The idea that this SNiP is “faulty” is an interesting one– it is perfectly possible that it is only a problem in the unhealthy environment of Western life, and that the gene variant has been preserves as it carries a survival advantage in less toxic environments.

We see this again and again- that a gene is labelled “the gene for cancer” or so forth- when logically speaking there should be no genes for dysfunction.
Sickle cell anaemia and thalassemia are great examples- the heterozygote confers survival advantages. So do the genes for Ashkenazi conditions like Tay Sach’s disease- it appears that the heterozygote confers higher intelectual processing speed- an advantage when your population is being systematically persecuted.

At last count humans have between 20,000 to 25,000 genes in the DNA of every cell. A few faulty genes can be expected.
According to the study “Our research strongly suggests alcohol and genetics are interacting”. Some people call this “epigenetics”, whereby gene expression (good or bad) is affected by conditions external to the nucleus: lead, mercury, aluminum, alcohol, food, chemicals, hyperglycaemia, hyperinsulinaemia, bad fats, stress etc. (stuff covered in this blog).

David Bailey – polysupplementism and “how does anyone select a subset to consume on a rational basis?”

Indeed! Since coming out of intensive care my list of supplements has increased greatly.

I suppose you could consider serum testing for deficiencies. But where to start?

The list would be endless. And many tests are quite complex e.g. see Dr Kendrick’s posts on magnesium and magnesium testing. Homocysteine levels might indicate a deficiency in certain vitamins. I seem to recall from my homocysteine serum test that it requires a special machine (I think) and you have to get your blood to the lab within 15 mins – that’s how it was for my test.

And many tests are not readily available – try getting your chondroitin sulphate levels checked if you bite into that CVD hypothesis. I drew a blank with that here in the UK.

And there is the cost too. I’d be surprised if your GP would do these for free, unless there was good reason. Therefore it’s self funding.

Possibly, I guess it’s using resources like this website and the info provided by both Dr Kendrick and the commenters. That’s how I came to take CoQ10, which I’d never heard of before. I knew all about heart ejection fractions though and someone provided links to Dr Peter Langsjoen’s talks on COQ10 and the efficacy of CoQ10 in strengthening the heart muscle. I take it all the time. No idea if I’m deficient or not…either I couldn’t find or afford a test.

Charles
I get that question all the time” a normal diet supplies all you need, how do you know it is necessary, does any good, etc etc”
My reply is on the grounds that what do they suggest, that I stop and start again in five years time when it will be too late. As for testing, I don’t bother. See the Mercola article on deaths from prescribed medicines in the states as opposed to vitamin and supplement overconsumption. The answer is about 100,000 as opposed to zero.

I try to stick mostly to extracts and superfoods. I’m leery of processed multivitamin type supplements. Taking nutrients out of their context is often problematical, I believe. For selenium, eat a couple of Brazil nuts.
By the way, for heart weakness, I think the herb Arjuna is more effective than COQ10, but it is not an either/or. I would take both.
At the same time, so many studies are done badly. Vitamin E needs to have its full complement of tocopherols. Synthetics don’t cut it. There are a lot of sneaky ways that diet studies and supplement studies are ruined.

There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.

Just to add to the discussion, I was referred to the Lipid clinic in our local hospital because of high cholesterol. It was measured at 9.2 and to quote from the consultant’s report “the difficulty is that so few people have cholesterol and HDL values similar to yours….” Having had a bad reaction to statins I decided to pay for a CT scan which came back with a calcium score of 0 (at age 64). So here is another black swan.

I have genetically diagnosed FH. I have followed a strict carnivore diet to treat Crohn’s disease for over two years. I will be 47 years old next month. My LDL usually is between 300-400mg/dl (more than 10mmol/l). A few years ago when my then-doctor tried to insist on statins despite all other health parameters being excellent, I took matters into my own hands. I went to the local heart center for a CT scan, got a perfect score. The doctor fired me as a patient and I never bothered to replace them. In following years I have also taken two trivascular ultrasound scans and received excellent scores as well, and all other health markers have continued to be excellent. Another black swan!

Hi Frederica, age has something to do with AF, a risk factor for many other things as well. Apoptosis and necrosis of aged cells happens on a regular basis. Apparently autophagy is beneficial for slowing down the aging process. Unfortunately this could lead into discussions about diet.

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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